Ischemic stroke is one of the most common neurological disorders. Oxidative stress, inflammation, and the reduction of Brain-Derived Neurotrophic Factor (BDNF) are implicated in cell death during ischemic stroke. Several studies suggest that Coenzyme Q10 (CoQ10) has antioxidant, anti-inflammatory, neuroprotective properties and can increase BDNF levels. This study investigated the effects of oral CoQ10 supplementation on oxidative stress biomarkers Total Antioxidant Capacity (TAC), Superoxide Dismutase (SOD), Malondialdehyde (MDA), Total Thiol Groups (TTG) - as well as serum levels of Interleukin-6 (IL-6) and BDNF in ischemic stroke patients.

Fifty patients hospitalized for acute ischemic stroke were randomly divided into two groups: placebo (n = 25) and CoQ10 (600 mg/day) supplementation (n = 25). The intervention began 24 hours after stroke onset and continued for 30 days.

Significant reductions in serum MDA and IL-6 levels, alongside increased SOD and BDNF levels, were observed in the CoQ10 group. No significant differences were found in TAC or TTG levels between the groups.

A 30-day regimen of CoQ10 (600 mg/day) resulted in reduced oxidative stress and inflammation, alongside increased BDNF, suggesting potential neuroprotective benefits for post-stroke rehabilitation. CoQ10 May be considered a therapeutic option for enhancing neuroprotection and rehabilitation in stroke patients.

Chronic Obstructive Pulmonary Disease (COPD) remains a serious public health problem globally, and the mortality rate for older COPD patients with cognitive impairment is almost three times that of older patients with cognitive impairment or COPD. The aim of this study was to construct a nomogram prediction model for the risk of comorbid cognitive impairment in COPD patients and to evaluate its clinical application. It helps to detect cognitive impairment in COPD patients at an early stage and give them effective interventions in time, so as to delay the progression of COPD patients and improve their prognosis.

In this study, patients with COPD hospitalized at the Affiliated Hospital of North China University of Science and Technology were evaluated for cognitive function using the Montreal Cognitive Assessment(MoCA) scale after stabilization of acute exacerbations. Participants were stratified into two groups: a case group (with cognitive impairment) and a control group (without cognitive impairment), based on predefined MoCA cutoff scores(< 26scores). Based on the basic characteristics of the patients and the laboratory indexes after stabilization of acute exacerbations, we conducted statistical analyses, screened out the risk factors and established the Nomogram Prediction Model by using the R software, and finally, we evaluated the clinical value of the model through the calculation of ROC curves for sensitivity, specificity and kappa value. Finally, the sensitivity, specificity and Kappa value were calculated by ROC curve to evaluate the clinical value of the model.

After statistical analysis, C-reactive protein (CRP) and homocysteine (Hcy) were found to be the risk factors for combined cognitive impairment in COPD patients, and the Nomogram prediction model was constructed by combining CRP and Hcy and plotted the ROC curve, and it was found that its model finally screened the critical value of the total score of 62.55, and the area under the ROC curve of the model was 0.870, and the sensitivity was 84.7%, and the specificity was 80.4%, indicating that it has a high degree of consistency with the actual results, which indicated that the consistency between the prediction results and the actual results was better, and it had a higher clinical application value.

CRP and Hcy are closely associated with comorbid cognitive impairment in COPD patients after stabilization of acute exacerbations, and increased levels of CRP and Hcy are associated with an increased risk of comorbid cognitive impairment in COPD patients. Combining both CRP and Hcy to create a nomogram model for predicting comorbid cognitive impairment in patients with COPD has good predictive ability.

Cognitive impairment is an important cause of disability and death among the elderly. One of the most important risk factors is stroke. Post-stroke cognitive impairment (PSCI) not only diminishes the quality of life for patients but also increases the burden on families and society. But PSCI can be mitigated through early intervention. Cerebral small vessel disease (CSVD) is one of the significant causes of stroke and has garnered considerable attention in PSCI. Therefore, this study aims to identify research priorities and trends in PSCI through bibliometric analysis, and further explore the role played by CSVD in PSCI.

In this study, we performed a systematic search in the Science Citation Index Expanded (SCI-E) of the Web of Science Core Collection (WoSCC). VOSviewer, CiteSpace and Origin were mainly used to visualize the research focus and trend in PSCI. In addition, we screened the retrieved literature again, and performed keyword analysis on the studies related to CSVD.

A total of 1,943 publications were retrieved in the field of PSCI in this study, with consistent upward trend in annual publications in recent years. Pendlebury was an important leader in PSCI research. Capital Medical University was in the leading position judging from the number of publications. China had the highest number of publications in this field. The journal Stroke had the strongest international influence in this field. Keywords such as "functional connectivity," "tool," "systematic review," and "meta-analysis" have been revealed to have momentous impact on PSCI in recent years. In the further analysis of PSCI and CSVD, "hypertension," "white matter hyperintensities (WMH)," "cerebral microbleeds (CMBs)," and "cerebral amyloid angiopathy (CAA)" received extensive attention.

The study of PSCI is still in the development stage. This study systematically summarizes the progress and development trend in the field of PSCI, and further explores the relationship between CSVD and PSCI through hypertension and magnetic resonance imaging markers. This study is of great significance for researchers to quickly understand the development of PSCI, but also helps them understand future directions, and provides important insights for the prevention and treatment of PSCI.

This study aims to assess the pattern of functional connectivity (FC) between cerebellar subregions, the basal ganglia (BG), and the cortex, and explore the relationship between FC patterns and cognitive function after stroke with BG infarcts.

A total of 39 stroke patients and 29 healthy controls were recruited. Four cerebellar seed points were selected, and the FC of each seed point with other voxels in the whole brain was calculated. FC and cognitive performance were compared between the two groups, and their correlations were analyzed.

Stroke patients exhibited increased FC between the bilateral cerebellum IX and BG (particularly the head of the caudate nucleus), which was positively correlated with episodic memory, visuospatial ability, and attention. Increased FC was also observed between the right cerebellum Crus I/II and BG, as well as the bilateral cerebellum VI and BG, correlating positively with episodic memory. Conversely, decreased FC was identified between the bilateral cerebellum IX and the right caudal cuneus, which negatively correlated with episodic memory, language, and attention but positively correlated with executive function. Additionally, increased FC between the bilateral cerebellum VI and the bilateral inferior parietal lobule was associated with improvements in episodic memory, language, and attention. Decreased FC was observed between the right cerebellum VI and the left insula, as well as between the right cerebellum Crus I/II and the left insula, which negatively correlated with episodic memory.

The enhanced FC between the cerebellum and BG, along with the reorganization of new neural circuits involving the cerebellar cortex, may contribute to cognitive recovery following stroke. These changes may represent compensatory mechanisms of the cerebellum in response to stroke injury.

Enhancing post-stroke cognitive impairment (PSCI) is a key aspect of prognosis for stroke patients. Low-frequency repetitive transcranial magnetic stimulation (LF-rTMS) is currently a widely utilised method for treating PSCI. With the increasing promotion of traditional Chinese medicine, Xingnao Kaiqiao (XNKQ) acupuncture has been progressively incorporated into clinical treatment. This paper observes the effect of LF-rTMS with XNKQ acupuncture on patients with PSCI.

Totally, 192 patients with PSCI were consecutively recruited and treated either with LF-rTMS and XNKQ acupuncture (observation group) or LF-rTMS only (control group) for 4 weeks. The pre- and post-treatment Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores, P300 latency and amplitude, inflammatory factor levels were compared and clinical efficacy was assessed.

Both groups exhibited increased MMSE/MoCA scores, and P300 amplitude, and shortened P300 latency, and the observation group had higher scores and P300 amplitude, and shorter P300 latency than the control group. Both groups displayed decreased inflammatory factor levels (Tumour necrosis factor-α, interleukin (IL)-6, IL-10, IL-1β) after treatment, which were lower in the observation group than the control group. Inflammatory factor levels in PSCI patients were negatively interrelated with MMSE, MoCA score and P300 amplitude, and positively with P300 latency. The observation group showed an increased number of patients showing cured and significantly effective results, a decreased number of patients showing effective and invalid results, and an observably elevated total effective rate.

LF-rTMS with XNKQ acupuncture can improve cognitive function and reduce inflammatory immune response, and has better clinical efficacy in PSCI patients.

Post-stroke cognitive impairment (PSCI) is a common and significant disorder affecting a considerable proportion of stroke patients. PSCI is a known factor that increases the risk of mortality, dependency, and institutionalization in stroke patients. The early prediction of PSCI and the implementation of cognitive rehabilitation could enhance the quality of life of stroke patients and reduce the burden on their families. It is therefore imperative to identify risk factors for PSCIs in the early stages of stroke and to implement early cognitive rehabilitation with an appropriate prognosis. A number of risk factors for PSCI can be identified in patient characteristics, clinical findings, and imaging findings. It is unfortunate that the majority of factors associated with PSCI are non-modifiable. However, the only modifiable factor that can be controlled is the management of stroke risk factors for secondary prevention. Further research is needed to elucidate the potential benefits of various cognitive rehabilitation programs for the prevention and improvement of PSCI.

The efficacy of DL-3-n-butylphthalide (NBP) in the treatment of post-stroke cognitive impairment (PSCI) has been reported previously. However, the course of treatment that shows curative effect and cytokines predictive of the efficacy of NBP in the treatment of PSCI have not been systematically evaluated. This study aimed to assess the efficacy, course of treatment, and cytokines that can predict the effectiveness of NBP in treating poststroke cognitive impairment PSCI.

This study has been registered with PROSPERO (registration number CRD42024518768). Randomized controlled trial (RCT) data dated by November 12, 2023 were retrieved from the PubMed, Embase, Cochrane Library, Web of Science, Wanfang, CNKI, CSTJ, and SinoMed databases using medical subject terms combined with free words. The updated Cochrane RoB-I Risk of Bias tool was utilized for literature quality evaluation. Statistical analysis were carried out using Review Manager 5.4.1 software.

Thirty-eight original studies involving 5417 PSCI patients were analyzed. The results showed that NBP had a beneficial impact on cognitive function in PSCI patients when used alone or in combination therapy, as assessed by the Mini-mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scale. The effect sizes were significant for both monotherapy and combination therapy. Subgroup analyses based on treatment cycle indicated that NBP enhanced cognitive function in PSCI patients from 1 week after intervention: MMSE (SMD = 0.43, 95% CI [0.28, 0.58], P < 0.001), MoCA (SMD = 0.44, 95% CI [0.27, 0.61], P < 0.001). There was a cumulative enhancement in cognitive function within 6 months after NBP treatment based on the MoCA scores (SMD = 0.61, 95% CI [0.30, 0.91], P < 0.001). Furthermore, decreased levels of the cytokines Hs-CRP, TNF-α, IL-6, IL-8, Hcy, NSE, MDA, MMP-9, and Cys-C (SMD = -2.28, 95% CI [-2.97, 1.58], P < 0.001) and increased levels of BDNF, VEGF, and TIMP-1 (SMD = 2.80, 95% CI [1.66, 3.94], P < 0.001) were also predictive of treatment efficacy.

NBP plays a beneficial role in improving cognitive function in PSCI patients, and their prognoses could be predicted by serum cytokine levels. However, high-quality, multicenter, multisample, and RCTs are still needed to confirm the clinical validity of NBP due to its low methodological quality.

This study aims to investigate how electroacupuncture regulates the learning and memory abilities of poststroke cognitive impairment (PSCI) rats through the TLR4/NF-κB/NLRP3 signaling pathway on the hippocampal microglia. Thirty male rats were randomly divided into three groups: sham surgery group, PSCI model group, and electroacupuncture group, with 10 rats in each group. Middle cerebral artery occlusion was used to establish the PSCI model. The Zea Longa method was used to score the rats' neurological function. Electroacupuncture was utilized for 21 days to improve PSCI. The learning and memory abilities of rats were tested using the Morris water maze. Hematoxylin-eosin staining and immunofluorescence were used to find the hippocampus' pathological changes. The concentration of interleukin-1β, interleukin-6, tumor necrosis factor-α, and interleukin-18 were detected by ELISA. The mRNA expression levels of associated inflammatory corpuscles were measured by quantitative real-time PCR. The protein expression levels of TLR4, MyD88, NF-κB, and NLRP3 were measured using western blotting. Electroacupuncture improved not only the learning and memory abilities of PSCI rats but also hippocampal morphology. Electroacupuncture inhibited the activation of microglia and the TLR4/NF-κB/NLRP3 signaling pathway. Electroacupuncture also reduced proinflammatory factors and restrained the mRNA levels of NLRP3-associated inflammatory cytokines. Its mechanism was related to inhibiting the expression of the TLR4/NF-κB/NLRP3 signaling pathway, attenuating the release of inflammatory factors, and regulating the activation of hippocampal microglia in the brain.

There are currently no effective prediction methods for evaluating the occurrence of cognitive impairment in patients with cerebral small vessel disease (CSVD).

To investigate the risk factors for cognitive dysfunction in patients with CSVD and to construct a risk prediction model.

A retrospective study was conducted on 227 patients with CSVD. All patients were assessed by brain magnetic resonance imaging (MRI), and the Montreal Cognitive Assessment (MoCA) was used to assess cognitive status. In addition, the patient's medical records were also recorded. The clinical data were divided into a normal cognitive function group and a cognitive impairment group. A MoCA score < 26 (an additional 1 point for education < 12 years) is defined as cognitive dysfunction.

A total of 227 patients (mean age 66.7 ± 6.99 years) with CSVD were included in this study, of whom 68.7% were male and 100 patients (44.1%) developed cognitive impairment. Age (OR = 1.070; 95% CI = 1.015 ~ 1.128, p < 0.05), hypertension (OR = 2.863; 95% CI = 1.438 ~ 5.699, p < 0.05), homocysteine(HCY) (OR = 1.065; 95% CI = 1.005 ~ 1.127, p < 0.05), lacunar infarct score(Lac_score) (OR = 2.732; 95% CI = 1.094 ~ 6.825, P < 0.05), and CSVD total burden (CSVD_score) (OR = 3.823; 95% CI = 1.496 ~ 9.768, P < 0.05) were found to be independent risk factors for cognitive decline in the present study. The above 5 variables were used to construct a nomogram, and the model was internally validated by using bootstrapping with a C-index of 0.839. The external model validation C-index was 0.867.

The nomogram model based on brain MR images and clinical data helps in individualizing the probability of cognitive impairment progression in patients with CSVD.

Post-stroke cognitive impairment (PSCI) is a frequent consequence of stroke, which affects the quality of life and prognosis of stroke survivors. Numerous studies have indicated that blood biomarkers may be the key determinants for predicting and diagnosing cognitive impairment, but the results remain varied. Therefore, this meta-analysis aims to summarize potential biomarkers associated with PSCI.

PubMed, Web of Science, Embase, and Cochrane Library were comprehensively searched for studies exploring blood biomarkers associated with PSCI from inception to 15 April 2022.

63 studies were selected from 4,047 references, which involves 95 blood biomarkers associated with the PSCI. We meta-analyzed 20 potential blood biomarker candidates, the results shown that the homocysteine (Hcy) (SMD = 0.35; 95 %CI: 0.20-0.49; P < 0.00001), c-reactive protein (CRP) (SMD = 0.49; 95 %CI: 0.20-0.78; P = 0.0008), uric acid (UA) (SMD = 0.41; 95 %CI: 0.06-0.76; P = 0.02), interleukin 6 (IL-6) (SMD = 0.92; 95 % CI: 0.27-1.57; P = 0.005), cystatin C (Cys-C) (SMD = 0.58; 95 %CI: 0.28-0.87; P = 0.0001), creatinine (SMD = 0.39; 95 %CI: 0.23-0.55; P < 0.00001) and tumor necrosis factor alpha (TNF-α) (SMD = 0.45; 95 %CI: 0.08-0.82; P = 0.02) levels were significantly higher in patients with PSCI than in the non-PSCI group.

Based on our findings, we recommend that paramedics focus on the blood biomarkers levels of Hcy, CRP, UA, IL-6, Cys-C, creatinine and TNF-α in conjunction with neuroimaging and neuropsychological assessment to assess the risk of PSCI, which may help with early detection and timely preventive measures. At the same time, other potential blood biomarkers should be further validated in future studies.

Patients experience post-stroke cognitive impairment during aging. To date, no specific treatment solution has been reported for this disorder.

The purpose of this study was to evaluate the effects of exercise training and coenzyme Q10 supplementation on middle cerebral artery occlusion (MCAO) induced behavioral impairment, long-term potentiation inhibition and cerebral infarction size in aging rats.

Fifty aging male rats underwent MCAO surgery and were randomly distributed in to the following groups: 1-Sham, 2- control, 3- Coenzyme Q10, 4- Exercise training and 5- Exercise training with Q10 supplementation (Ex + Q10). Aerobic training groups were allowed to run on a treadmill for 12 weeks. Q10 (50 mg/kg) was administered intragastrically by gavage. Morris water maze, shuttle box and elevated plus maze tests were used to evaluate cognitive function. The population spike (PS) amplitude and slope of excitatory postsynaptic potentials (EPSP) in the dentate gyrus area were recorded as a result of perforant pathway electrical stimulation.

Our study showed that Q10 and aerobic training alone ameliorate spatial memory in the acquisition phase, but have no effect on spatial memory in the retention phase. Q10 and exercise training synergistically promoted spatial memory in the retention phase. Q10 and exercise training separately and simultaneously mitigated cerebral ischemia-induced passive avoidance memory impairment in acquisition and retention phases. The EPSP did not differ between the groups, but exercise training and Q10 ameliorate the PS amplitude in hippocampal responses to perforant path stimulation. Exercising and Q10 simultaneously reduced the cerebral infarction volume.

Collectively, the findings of the present study imply that 12 weeks of aerobic training and Q10 supplementation alone can simultaneously reverse cerebral ischemia induced neurobehavioral deficits via amelioration of synaptic plasticity and a reduction in cerebral infarction volume in senescent rats.

Post-stroke cognitive impairment is one of the major causes of disability due to cerebral ischemia. MAD2B is an inhibitor of Cdh1/APC, and loss of Cdh1/APC function in mature neurons increases ROCK2 activity, leading to changes in synaptic plasticity and memory loss in mouse neurons. Whether MAD2B regulates learning memory capacity through ROCK2 in cerebral ischemia is not known.

We investigated the role and mechanism of MAD2B in cerebral ischemia-induced cognitive dysfunction.

The expression of MAD2B and its downstream related molecules was detected by immunoblotting and intervened with neuroprotectants after middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R). We constructed MAD2B-cKO-specific knockout mice, knocked down and overexpressed MAD2B in mouse hippocampus by lentiviral injection in brain stereotaxis, modeled cerebral ischemia by using MCAO, and explored the role of MAD2B in post-stroke cognitive impairment (PSCI) by animal behaviors such as Y-maze and Novel object recognition test. Then the expression of MAD2B/ROCK2, downstream molecules and apoptosis-related molecules was detected. Finally, ROCK2 expression was intervened using its inhibitor and shRNA-ROCK2 lentivirus.

The expression of MAD2B and its downstream molecules increased after MCAO and OGD/R. Nonetheless, this expression underwent a decline post-therapy with neuroprotective agents. Deletion of MAD2B in the hippocampus ameliorated memory and learning deficits and improved motor coordination in MCAO mice. Conversely, the overexpression of MAD2B in the hippocampus exacerbated learning and memory deficits. Deletion of MAD2B resulted in the downregulation of ROCK2/LIMK1/cofilin. It effectively reduced ischemia-induced upregulation of BAX and cleaved caspase-3, which could be reversed by MAD2B overexpression. Inhibition or knockdown of ROCK2 expression in primary cultured neurons led to the downregulation of LIMK1/cofilin expression and reduced the expression of apoptosis-associated molecules induced by ischemia.

Our findings suggest that MAD2B affects neuronal apoptosis via Rock2, which affects neurological function and cerebral infarction.

This review aimed to assess the impact of different exercise dosages on cognitive function in individuals with post-stroke cognitive impairment (PSCI).

Four electronic databases-Embase, PubMed, Web of Science, and Cochrane Library-were systematically searched from inception to 01 January 2024, focusing on the impact of exercise therapy on cognitive function in individuals with PSCI. Only randomized controlled trials meeting the criteria were included. The exercise therapy dose and adherence were evaluated following the American College of Sports Medicine (ACSM) guidelines, categorized into a high compliance group with ACSM recommendations and a low or uncertain compliance group. A random-effects model compared the effect of ACSM compliance on cognitive function in individuals with PSCI, with the effect size represented by the standardized mean difference (SMD) and a 95% confidence interval (CI).

In total, 18 studies meeting the criteria were included, with data from 1,742 participants. The findings suggested a beneficial effect of exercise on cognitive function in individuals with PSCI [SMD = 0.42, 95% CI (0.20, 0.65)]. Ten studies were categorized as the "high adherence group" and eight in the "low or uncertain adherence group" based on the ACSM recommendations. The subgroup analysis revealed that the SMD of the high compliance group was 0.46 (95% CI: 0.10, 0.82) (p = 0.01), while the SMD of the low or uncertain compliance group was 0.38 (95% CI: 0.07, 0.70) (p = 0.02).

Our study indicates the beneficial impact of exercise for patients with PSCI over no exercise. Furthermore, high adherence to the exercise dose recommended by ACSM guidelines demonstrated a more substantial improvement in cognitive function than low or uncertain adherence in patients with PSCI. Systematic Review Registration: https:// www.crd.york.ac.uk/prospero/#myprospero, identifier CRD42023487915.

Post-stroke cognitive impairment (PSCI) is a common decline in cognitive abilities that occurs within 3 months after a stroke. During recovery, stroke survivors often experience varying degrees of cognitive decline, with some patients experiencing permanent cognitive deficits. Thus, it is crucial to prioritise recovery and rehabilitation after a stroke to promote optimal protection of and improvement in cognitive function. Honey derived from stingless bees has been linked to various therapeutic properties, including neuroprotective effects. However, scientific evidence for the mechanisms through which these honey supplements enhance cognitive function remains limited. This narrative review aims to provide an overview of the causes of PSCI, current treatments, the biomarkers influencing cognition in post-stroke patients and the potential of stingless bee honey (SBH) as a neuroprotective agent against the progression of PSCI.

This trial analyzed high-sensitivity C-reactive protein (hs-CRP), homocysteine (Hcy), and macrophage migration inhibitory factor (MIF) level in serum and their correlation with symptom severity and cognitive function in patients with schizophrenia (SP).

Sixty-eight SP patients were enrolled in the SP group, and 68 healthy volunteers were in the control (CN) group. Serum hs-CRP, Hcy, and MIF were measured, and symptom severity was assessed with the Positive and Negative Symptom Scale (PANSS). Cognitive function was determined with the MATRICS Consensus Cognitive Battery (MCCB). The SP group was divided into high PANSS score (PANSS ≥70 points) and low PANSS score (PANSS <70 points), or the mild cognitive dysfunction group and severe cognitive dysfunction group according to the median MCCB score. The correlation between serum hs-CRP, Hcy, and MIF levels and PANSS and MCCB scores in SP patients was examined by Pearson correlation analysis.

SP patients had higher serum hs-CRP, Hcy, and MIF levels and showed higher PANSS scores and lower MCCB total score. Serum hs-CRP, Hcy, and MIF levels in the high PANSS group were higher than those in the low PANSS group and in the severe cognitive dysfunction group than in the mild cognitive dysfunction group. Serum hs-CRP, Hcy, and MIF levels in SP patients were positively correlated with PANSS total score and negatively correlated with MCCB total score.

High serum hs-CRP, Hcy, and MIF levels in SP patients are correlated with symptom severity and cognitive dysfunction.

The reliability of clinical evidence depends on high-quality meta-analyses/ systematic reviews (MAs/SRs). However, there has been no assessment of the quality of MAs/SRs for repetitive transcranial magnetic stimulation (rTMS) in post-stroke cognitive impairment (PSCI), both nationally and internationally. This article seeks to use radar plotting to visually present the quality of MAs/SRs on rTMS for improving cognitive function in PSCI, aiming to offer an intuitive foundation for clinical research.

Eight Chinese or English databases were systematically searched to collect comprehensive literature, and the retrieval time ranged from inception to 26 March 2024. Literature ranking was calculated using six dimensions: publication year, design type, AMSTAR-2 score, PRISMA score, publication bias, and homogeneity. Finally, radar plots were drafted to present a multivariate literature evaluation. The GRADE tool assessed the strength of evidence for the outcome indicators included in the MAs/SRs.

The 17 articles included had average scores of 12.29, 17, 9.88, 9.71, 12.88, and 12.76 for each dimension. The radar plot showed that an article published in 2023 had the highest rank and a large radar plot area, while an article published in 2021 had the lowest rank and a small radar plot area. The GRADE tool evaluation revealed that 51 pieces of evidence were of very low quality, 67 were of low quality, 12 were of moderate quality, and only one was of high quality.

The average rank score of literature ranged from 8.50 to 17, with higher rankings indicating greater significance in literature reference. Variations in literature quality were attributed to inadequate study planning, irregular literature search and screening, insufficient description of inclusion criteria for studies, and inadequate consideration of bias risk in the included studies. Most MAs/SRs indicated that rTMS was more effective than the control group in enhancing the global cognitive function and activities of daily living in PSCI patients. However, the overall quality of the literature was generally low and needs validation from future high-quality evidence.Systematic review registration:https://www.crd.york.ac.uk/prospero/, identifier CRD42023491280.

Motor impairment is one of the most common defects after stroke, which could seriously affect the life quality of stroke patients. Exercise intervention gradually becomes a popular alternative rehabilitation therapy because of its safety and applicability.

To systematically assess the effect of Qigong exercise on motor function in stroke patients.

Randomized controlled trials that evaluated the effect of Qigong on motor function of stroke patients were obtained from PubMed and Chinese National Knowledge Infrastructure through May 2022. Mean values and standard deviations of the post-intervention score in both experimental group and control group were collected to calculate the mean difference (MD) and corresponkding 95% confidence interval (95% CI) of each study, which were quantificationally summarized using the Review Manager 5.3 software.

Nineteen randomized controlled trials enrolling 1487 stroke patients were included. Pooled results indicated that Qigong exercise had beneficial effect on balance function (Berg Balance Scale [MD: 7.56, 95% CI: 4.09-11.02]), limb motor function (Fugl-Meyer Assessment [total score: MD: 7.54, 95% CI: 6.38-8.69; upper limb: MD: 3.57, 95% CI: 0.71-6.43; lower limb: MD: 2.44, 95% CI: 0.59-4.29]) and walking function (6-min walking test [MD: 62.21, 95% CI: 11.70-112.73]) of stroke patients. It was also found to be associated with an improvement in trunk function as indicated by the Trunk Impairment Scale.

Available evidence supported potential benefits of Qigong exercise for improving motor functions of stroke patients. As a safe and widely applicable exercise, Qigong is worthy of further promotion in the rehabilitation of stroke patients.

Autophagy-related gene (ATG) 5 regulates blood lipids, chronic inflammation, CD4+ T-cell differentiation, and neuronal death and is involved in post-stroke cognitive impairment. This study aimed to explore the correlation of serum ATG5 with CD4+ T cells and cognition impairment in stroke patients. Peripheral blood was collected from 180 stroke patients for serum ATG5 and T helper (Th) 1, Th2, Th17, and regulatory T (Treg) cell detection via enzyme-linked immunosorbent assays and flow cytometry. The Mini-Mental State Examination (MMSE) scale was completed at enrollment, year (Y)1, Y2, and Y3 in stroke patients. Serum ATG5 was also measured in 50 healthy controls (HCs). Serum ATG5 was elevated in stroke patients compared to HCs (P<0.001) and was positively correlated to Th2 cells (P=0.022), Th17 cells (P<0.001), and Th17/Treg ratio (P<0.001) in stroke patients but not correlated with Th1 cells, Th1/Th2 ratio, or Treg cells (all P>0.050). Serum ATG5 (P=0.037), Th1 cells (P=0.022), Th17 cells (P=0.002), and Th17/Treg ratio (P=0.018) were elevated in stroke patients with MMSE score-identified cognition impairment vs those without cognition impairment, whereas Th2 cells, Th1/Th2 ratio, and Treg cells were not different between them (all P>0.050). Importantly, serum ATG5 was negatively linked with MMSE score at enrollment (P=0.004), Y1 (P=0.002), Y2 (P=0.014), and Y3 (P=0.001); moreover, it was positively related to 2-year (P=0.024) and 3-year (P=0.012) MMSE score decline in stroke patients. Serum ATG5 was positively correlated with Th2 and Th17 cells and estimated cognitive function decline in stroke patients.

Our research aims to elucidate the significance of type 2 diabetes (T2D) and provides an insight into a novel risk model for post-cerebral infarction cognitive dysfunction (PCICD).

Our study recruited inpatients hospitalized with cerebral infarction in Xijing hospital, who underwent cognitive assessment of Mini-Mental State Examination (MMSE) from January 2010 to December 2021. Cognitive status was dichotomized into normal cognition and cognitive impairment. Collected data referred to Demographic Features, Clinical Diseases, scale tests, fluid biomarkers involving inflammation, coagulation function, hepatorenal function, lipid and glycemic management.

In our pooled dataset from 924 eligible patients, we included 353 in the final analysis (age range 65-91; 30.31% female). Multivariate logistic regression analysis was performed to show that Rural Areas (OR = 1.976, 95%CI = 1.111-3.515, P = 0.020), T2D (OR = 2.125, 95%CI = 1.267-3.563, P = 0.004), Direct Bilirubin (OR = 0.388, 95%CI = 0.196-0.769, P = 0.007), Severity of Dependence in terms of Barthel Index (OR = 1.708, 95%CI = 1.193-2.445, P = 0.003) that were independently associated with PCICD, constituting a model with optimal predictive efficiency.

To the best of our knowledge, this study provides a practicable map of strategical predictors to robustly identify cognitive dysfunction at risk of post-cerebral infarction for clinicians in a broad sense. Of note, our findings support that the decline in serum direct bilirubin (DBil) concentration is linked to protecting cognitive function.

This pilot study in post-stroke patients evaluated the effects of supplementation with Pycnogenol® on alterations in cognitive functions (COFU) over a period of 6 months, starting 4 weeks after the stroke.

The effects of supplementation - possibly acting on residual brain edema, on global cognitive function, attention and on mental performance - were studied. A control group used standard management (SM) and the other group added Pycnogenol®, 150 mg daily to SM.

38 post-stroke patients completed the 6-month-study, 20 in the Pycnogenol® group and 18 in the control group. No side effects were observed with the supplement. The tolerability was very good. The patients included into the two groups were comparable for age, sex and clinical distribution. There were 2 dropouts in the control group, due to non-medical problems. Main COFU parameters (assessed by a cognitive questionnaire) were significantly improved (all single items) with the supplement compared to controls (P<0.05). Additional observations indicate that Pycnogenol® patients experienced significantly less mini-accidents (including falls) than controls (P<0.05). The incidences of (minor) psychotic episodes or conflicts and distress and other problems including rare occurrence of minor hallucinations, were lower with the supplementation than in controls (P<0.05). Single observations concerning daily tasks indicated a better effect of Pycnogenol® compared to controls (P<0.05). Plasma free radicals also decreased significantly with the supplement in comparison to controls (P<0.05). Globally, supplemented subjects had a better recovery than controls.

In post-stroke subjects, Pycnogenol® supplementation resulted in better recovery outcome and faster COFU 'normalization' after the stroke in comparison with SM; it can be considered a safe, manageable post-stroke, adjuvant management possibly reducing local brain edema. Nevertheless, more patients and a longer period of evaluation are needed to confirm these results.

Over the past decade, the stroke literature has begun to acknowledge and explore explanations for longstanding racial/ethnic differences in stroke outcomes. Poststroke cognitive impairment (PSCI) and poststroke aphasia are two such negative poststroke outcomes where racial/ethnic differences exist. Physiological differences, such as stroke type and lesion size, have been used to partially explain the variation in PSCI and aphasia. However, there is some evidence, although limited, that suggests neuroinflammatory processes as part of allostatic load may be a key contributor to the observed disparities.

In this tutorial, we explore the influence of race differences in inflammation on poststroke cognitive outcomes. We suggest lifetime stress and other external determinants of health such as neighborhood environment and discriminatory practices through "weathering" explain differences in inflammation. While using an allostatic load framework, we explore the literature focusing specifically on the role of neuroinflammation on poststroke outcomes.

Examination of the immune response poststroke provides a foundation for understanding the mechanisms of PSCI and poststroke aphasia and the potential contributions of neuroinflammatory processes on poststroke cognitive outcomes. Furthermore, understanding of racial differences in those processes may contribute to a better understanding of racial disparities in general stroke outcomes as well as poststroke aphasia.

The gut microbiome interacts with the brain bidirectionally through the microbiome-gutbrain axis, which plays a key role in regulating various nervous system pathophysiological processes. Trimethylamine N-oxide (TMAO) is produced by choline metabolism through intestinal microorganisms, which can cross the blood-brain barrier to act on the central nervous system. Previous studies have shown that elevated plasma TMAO concentrations increase the risk of major adverse cardiovascular events, but there are few studies on TMAO in cerebrovascular disease and vascular cognitive impairment. This review summarized a decade of research on the impact of TMAO on stroke and related cognitive impairment, with particular attention to the effects on vascular cognitive disorders. We demonstrated that TMAO has a marked impact on the occurrence, development, and prognosis of stroke by regulating cholesterol metabolism, foam cell formation, platelet hyperresponsiveness and thrombosis, and promoting inflammation and oxidative stress. TMAO can also influence the cognitive impairment caused by Alzheimer's disease and Parkinson's disease via inducing abnormal aggregation of key proteins, affecting inflammation and thrombosis. However, although clinical studies have confirmed the association between the microbiome-gut-brain axis and vascular cognitive impairment (cerebral small vessel disease and post-stroke cognitive impairment), the molecular mechanism of TMAO has not been clarified, and TMAO precursors seem to play the opposite role in the process of poststroke cognitive impairment. In addition, several studies have also reported the possible neuroprotective effects of TMAO. Existing therapies for these diseases targeted to regulate intestinal flora and its metabolites have shown good efficacy. TMAO is probably a new target for early prediction and treatment of stroke and vascular cognitive impairment.

Post-stroke cognitive impairment (PSCI) is a very common complication of ischemic stroke (IS). Triglyceride-glucose (TyG) index was an effective alternative marker of insulin resistance (IR). This prospective study was designed to explore the correlation between TyG index and PSCI.

Between January 1 2021 to June 30 2022, consecutive patients with first onset IS were enrolled prospectively. Baseline information was collected at admission and fasting blood was drawn the next morning. Montreal Cognitive Assessment (MoCA) was used to evaluate cognitive function at three months after stroke. Multiple regression analysis was used to explore the correlation between PSCI and TyG. Receiver operating characteristic (ROC) was performed to evaluate the predictive ability.

Ultimately, 313 patients were enrolled in this study. The TyG index was higher in patients with PSCI than those without PSCI (8.99 (8.55, 9.54) vs. 8.61(8.25, 8.87), P<0.001). The spearman correlation analysis indicated that TyG index was negatively correlated with MoCA score (r=-0.272, P<0.001). The multivariate logistic regression analysis demonstrated that TyG index was correlated with PSCI independently (P<0.001) regardless of whether the patients had diabetes or not. The area under curve (AUC) of the ROC was 0.684 (95%CI=0.635-0.768, P<0.001). The optimal cutoff value of TyG index for predicting PSCI was 8.81, with a sensitivity of 61.7% and a specificity of 73.6%.

A higher TyG index level at admission was independently correlated with increased risk of PSCI three months later and could be used as a predictor.

Cerebral apoplexy patients are prone to cognitive impairment, and it is very important to choose appropriate treatment methods to improve their cognitive impairment after stroke.

To evaluate the effects of enhanced external counterpulsation (EECP) in conjunction with atorvastatin on cognitive function, neurotransmitter levels, and the repair of brain tissue damage in patients with cognitive impairment due to stroke.

In this retrospective study, data from 60 patients with poststroke cognitive impairment due to stroke who were treated in our hospital from February 2021 to July 2022 were analyzed and divided into a treatment group (n = 30) and a control group (n = 30) according to the different nursing methods applied. Patients in the treatment group received EECP in addition to atorvastatin, while those in the control group received atorvastatin alone. Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and activities of daily living (ADL) scale scores were compared between the two groups. Additionally, the two groups were compared in terms of serum acetylcholine (ACh), acetylcholinesterase (AChE), nitric oxide (NO), endothelin-1 (ET-1), β2-microglobulin (β2-MG), glial fibrillary acidic protein (GFAP), and visinin-like protein 1 (VILIP-1) in the serum. Blood flow measurements from the anterior cerebral artery (ACA), middle cerebral artery (MCA) and posterior cerebral artery (PCA) were compared between the two groups before and after treatment, and the pulsatility index (PI) and resistance index (RI) of each artery were determined.

MMSE, MoCA, and ADL scores all improved in both groups following treatment, with the study group showing more improvement than the control group (P < 0.05). After treatment, there were statistically significant increases in both ACh and NO levels, whereas decreases occurred in AChE, ET-1, β2-MG, VILIP-1, and GFAP, levels and the PI and RI of the left-ACA, right-ACA, left-MCA, right-MCA, left-PCA, and right-PCA. The study group showed greater gains in all metrics than the control group (P < 0.05).

EECP combined with atorvastatin is effective in the treatment of cognitive impairment after stroke and can effectively improve the cognitive function, neurotransmitter levels, and brain tissue damage status of patients.

Stroke is the third leading cause of death and long-term disability in the world. Considered largely a disease of aging, its global economic and healthcare burden is expected to rise as more people survive into advanced age. With recent advances in acute stroke management, including the expansion of time windows for treatment with intravenous thrombolysis and mechanical thrombectomy, we are likely to see an increase in survival rates. It is therefore critically important to understand the complete pathophysiology of ischemic stroke, both in the acute and subacute stages and during the chronic phase in the months and years following an ischemic event. One of the most clinically relevant aspects of the chronic sequelae of stroke is its extended negative effect on cognition. Cognitive impairment may be related to the deterioration and dysfunctional reorganization of white matter seen at later timepoints after stroke, as well as ongoing progressive neurodegeneration. The vasculature of the brain also undergoes significant insult and remodeling following stroke, undergoing changes which may further contribute to chronic stroke pathology. While inflammation and the immune response are well established drivers of acute stroke pathology, the chronicity and functional role of innate and adaptive immune responses in the post-ischemic brain and in the peripheral environment remain largely uncharacterized. In this review, we summarize the current literature on post-stroke injury progression, its chronic pathological features, and the putative secondary injury mechanisms underlying the development of cognitive impairment and dementia. We present findings from clinical and experimental studies and discuss the long-term effects of ischemic stroke on both brain anatomy and functional outcome. Identifying mechanisms that occur months to years after injury could lead to treatment strategies in the chronic phase of stroke to help mitigate stroke-associated cognitive decline in patients.

Translocator protein (TSPO) is a biomarker of neuroinflammation and brain injury. This study aimed to ascertain the potential of serum TSPO as a predictor of cognitive impairment after acute intracerebral hemorrhage (ICH).

In this prospective observational cohort study, 276 patients with supratentorial ICH were randomly assigned to two groups (184 patients in the study group and 92 in the validation group) in a 2:1 ratio. Serum TSPO levels were gauged at admission, and cognitive status was assessed using the Montreal Cognitive Assessment Scale (MoCA) post-stroke 3 months. A MoCA score of < 26 was considered indicative of cognitive impairment.

Serum TSPO levels were inversely correlated with MoCA scores (ρ=-0.592; P<0.001). Multivariate linear regression analysis showed that serum TSPO levels were independently associated with MoCA scores (β, -0.934; 95% confidence interval (CI), -1.412--0.455; VIF, 1.473; P<0.001). Serum TSPO levels were substantially higher in patients with cognitive impairment than in the remaining patients (median, 2.7 versus 1.6 ng/mL; P<0.001). Serum TSPO levels were linearly correlated with the risk of cognitive impairment under a restricted cubic spline (P=0.325) and independently predicted cognitive impairment (odds ratio, 1.589; 95% CI, 1.139-2.216; P=0.016). Subgroup analysis showed that the relationship between serum TSPO levels and cognitive impairment was not markedly influenced by other parameters, such as age, sex, drinking, smoking, hypertension, diabetes mellitus, body mass index, and dyslipidemia (all P for interaction > 0.05). The model, which contained serum TSPO, National Institutes of Health Stroke Scale scores and hematoma volume, performed well under the receiver operating characteristic curve, calibration curve and decision curve, and using the Hosmer-Lemeshow test. This model was validated in the validation group.

Serum TSPO level upon admission after ICH was independently associated with cognitive impairment, substantializing serum TSPO as a reliable predictor of post-ICH cognitive impairment.

Vascular cognitive impairment (VCI) has an increasing prevalence worldwide, accounting for at least 20%-40% of all diagnoses of dementia. The decline in cognitive function seriously impairs patients' activities of daily living and social participation and reduces their quality of life. However, there is still a lack of advanced, definitive rehabilitation programmes for VCI. Hyperbaric oxygen therapy (HBOT) and repetitive transcranial magnetic stimulation (rTMS) are recognised treatments for improving cognitive impairment. The former can restore oxygen supply in the brain by increasing oxygen partial pressure in brain tissue, while the latter can enhance neuronal excitability and promote synaptic plasticity. However, no studies have explored the effect of HBO combined with rTMS on VCI.

This study is designed as a single-centre, assessor-blind, randomised controlled clinical trial with four parallel arms. A total of 72 participants will be recruited and randomly assigned to the control group, HBOT group, rTMS group and HBOT combined with rTMS group at a ratio of 1:1:1:1. All enrolled participants will receive conventional treatment. The entire intervention period is 4 weeks, with a 3-week follow-up. Outcomes will be measured at baseline (T0), after a 4-week intervention (T1) and after an additional 3-week follow-up period (T2). The primary endpoint is the Montreal Cognitive Assessment score. The secondary endpoints are Mini-Mental State Examination score, Modified Barthel Index score, latency and amplitude of P300, cerebral cortical oxygenated haemoglobin (HbO2) and deoxygenated haemoglobin (HbR) concentrations as measured by task-state functional near-infrared spectroscopy.

Ethics approval was obtained from the West China Hospital Clinical Trials and Biomedical Ethics Committee of Sichuan University (ethics reference: 2022 (1972)). The findings will be published in peer-reviewed journals and disseminated through scientific conferences and seminars.

ChiCTR2300068242.

High-mobility group protein box 1 (HMGB1) is a cytokine with multiple functions (according to its subcellular location) that serves a marker of inflammation. CSF HMGB1 could be the part of pathological mechanisms that underlie the complications associated with CNS diseases. HMGB1 actively or passively released into the CSF is detected in the CSF in many diseases of the central nervous system (CNS) and thus may be useful as a biomarker. Pathological alterations in distant areas were observed due to lesions in a specific region, and the level of HMGB1 in the CSF was found to be elevated. Reducing the HMGB1 level via intraventricular injection of anti-HMGB1 neutralizing antibodies can improve the outcomes of CNS diseases. The results indicated that CSF HMGB1 could serve as a biomarker for predicting disease progression and may also act as a pathogenic factor contributing to pathological alterations in distant areas following focal lesions in the CNS. In this mini-review, the characteristics of HMGB1 and progress in research on CSF HMGB1 as a biomarker of CNS diseases were discussed. CSF HMGB1 is useful not only as a biomarker of CNS diseases but may also be involved in interactions between different brain regions and the spinal cord.

Ischemic stroke, a severe disease with high disability and mortality, causes an overburden in society and demands more effective treatments. Early rehabilitation and nursing intervention (ERNI) helps the postoperative recovery of patients with hypertensive intracerebral hemorrhage. However, the effect of ERNI on the recovery of people after ischemic stroke remains unclear.

Patients were treated with the ERNI program; subsequently, Mini-Mental State Examination, National Institute of Health stroke scale, Fugl-Meyer Assessment Scale, Daily living activity assessment, and Quality of life test were performed after the treatment of ERNI to evaluate the influence of ERNI on the cognitive function, motor function, and life quality of patients after ischemic stroke.

We observed that following the treatment of ERNI, cognitive, neurological, and motor functions, daily life qualities, and life quality in the ERNI-treated group were significantly better than that in the control group.

ERNI promoted the recovery of neurological function and improved the life qualities of patients after ischemic stroke.

Metabolites are reliable biomarkers for many diseases. However, their role in acute ischemic stroke (AIS) pathogenesis is not well understood. In this systematic review we aim to evaluate the current literature on the presence of metabolites in thrombi retrieved by mechanical thrombectomy from AIS patients. Following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) 2020 guidelines, we searched OVID Medline, PubMed, OVID Embase, Scopus, and Web of Science until July 13, 2022. Metabolites lists were extracted, and pathway analysis was performed in MetaboAnalyst database. Four articles listing metabolites were included in this systematic review. D-Glucose, diacylglycerol, phytosphingosine, galabiosylceramide, glucosylceramide and 4-hydroxynonenal were reported to be associated with clots. Metabolomics data analysis showed that glycolysis, lactose, and sphingolipid metabolism pathways were enriched. In conclusion, results of the present study show that the thrombi niche has a glycolytic phenotype. Future studies should work to better understand the metabolic properties of AIS thrombi.

Post-stroke cognitive impairment (PSCI) is one of the serious complications of stroke. The Montreal Cognitive Assessment (MoCA), as a brief cognitive impairment screening tool, is widely used in stroke survivors. However, some studies have suggested that the use of the universal cutoff value of 26 may be inappropriate for detecting cognitive impairments in stroke settings.

We conducted this study to identify the optimal cutoff value of the MoCA in screening for PSCI.

PubMed, CINAHL, Embase, the Cochrane Library, and Web of Science were searched for eligible studies until March 23, 2023. All studies were screened by two independent researchers. The quality of each article was evaluated by the Quality Assessment of Diagnostic Accuracy Studies-2 tool. A bivariate mixed-effects model was used to pool sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and the summary receiver operating characteristic curve.

Twenty-four studies with a total of 4231 patients were included in this review. Despite the lack of evidence of publication bias, a high degree of heterogeneity was observed. A meta-analysis revealed that a cutoff value of 21/22 yielded the best diagnostic accuracy. The optimal cutoff varied in different regions, stroke types, and stroke phases as well.

The optimal cutoff of MoCA was 21/22 for stroke populations rather than the initially recommended cutoff of 26. A revised (lower) cutoff should be considered for stroke survivors.

Total saponins from Trillium tschonoskii Maxim (TSTT), a bioactive component of local natural herbs in the Enshi area, China, have been demonstrated to have functions of restoring cognitive capacity and promoting axonal regeneration post-stroke, but the mechanism of this process remains unclear. The hippocampus is a critical tissue for controlling learning and memory capacity, and the sonic hedgehog (Shh) signaling pathway plays a major role in the patterning and synaptic plasticity of hippocampal neural circuits. Therefore, we aimed to investigate whether TSTT could restore learning and cognitive functions by modulating the Shh pathway in rats with post-stroke cognitive impairment (PSCI). The ischemia model was established by permanent middle cerebral artery occlusion (MCAO) in 100 Sprague-Dawley (SD) rats, and the model rats were administered using TSTT (100 mg/kg) or donepezil hydrochloride as the positive control (daily 0.45 mg/kg, DON) for 4 weeks after the operation. As assessed by the Morris water maze test, the cognitive function of PSCI rats was significantly improved upon TSTT treatment. Meanwhile, the cerebral infarct volume reduced with TSTT, as shown by HE and TTC staining, and the number of Nissl bodies and dendritic spine density were significantly increased, as shown by Nissl and Golgi staining. In addition, TSTT upregulated PSD-95, SYN, and GAP-43, and inhibited neuronal apoptosis, as evidenced by increased Bcl-2 levels along with decreased Bax and caspase-3 expression. TSTT could also significantly upregulate Shh, Ptch1, Smo, and Gli1 proteins, indicating the activation of the Shh signaling pathway. Therefore, TSTT can protect PSCI rats by inhibiting apoptosis and promoting neuronal synaptic remodeling. The Shh pathway is also involved.

Ischemic stroke is one of the major causes of human morbidity and mortality. The pathophysiology of ischemic stroke involves complex events, including oxidative stress and inflammation, that lead to neuronal loss and cognitive deficits. Palmatine (PAL) is a naturally occurring (Coptidis rhizome) isoquinoline alkaloid that belongs to the class of protoberberines and has a wide spectrum of pharmacological and biological effects. In the present study, we evaluated the impact of Palmatine on neuronal damage, memory deficits, and inflammatory response in mice submitted to permanent focal cerebral ischemia induced by middle cerebral artery (pMCAO) occlusion. The animals were treated with Palmatine (0.2, 2 and 20 mg/kg/day, orally) or vehicle (3% Tween + saline solution) 2 h after pMCAO once daily for 3 days. Cerebral ischemia was confirmed by evaluating the infarct area (TTC staining) and neurological deficit score 24 h after pMCAO. Treatment with palmatine (2 and 20 mg/kg) reduced infarct size and neurological deficits and prevented working and aversive memory deficits in ischemic mice. Palmatine, at a dose of 2 mg/kg, had a similar effect of reducing neuroinflammation 24 h after cerebral ischemia, decreasing TNF-, iNOS, COX-2, and NF- κB immunoreactivities and preventing the activation of microglia and astrocytes. Moreover, palmatine (2 mg/kg) reduced COX-2, iNOS, and IL-1β immunoreactivity 96 h after pMCAO. The neuroprotective properties of palmatine make it an excellent adjuvant treatment for strokes due to its inhibition of neuroinflammation.

Cognitive decline (CD) is devastating with a high incidence in patients after stroke. Although some studies have explored underlying associations between C-reactive protein (CRP) levels and cognitive decline after stroke, consistent results have not been obtained. Therefore, this meta-analysis aimed to explore whether or not higher levels of C-reactive proteins were associated with an increased risk of cognitive decline after stroke. To this end, PubMed, Embase, the Cochrane Library, and Web of Science were searched for eligible studies, and pooled effect sizes from eligible studies were calculated using random effect models. Furthermore, subgroups were established and meta-regression analyses were performed to explain the causes of heterogeneity. Eventually, nine studies with 3893 participants were included. Our statistical results suggested that the concentrations of peripheral CRP may be significantly increased for CD patients after stroke, compared to those of non-CD patients. Subgroup analyses showed that CRP was higher in CD than that in non-CD patients when the mini-mental state examination was used. A higher level of CRP in the acute phase of ischemic stroke may suggest an increased risk of CD after stroke. However, these results should be cautiously interpreted because of the limited sample sizes and the diversity of potential confounders in the studies included in this meta-analysis.

Background: Depressive symptoms have been associated with cognitive impairment after stroke, and women may be specifically affected. Objective: The aim of this study was to investigate gender-specific characteristics in the relationship between changes in depression severity and changes in cognitive performance after stroke. Methods: We prospectively evaluated 73 patients without a previous history of depression in the first and fourth months after a first ischemic stroke. The severity of depressive symptoms was assessed using the 31-item version of the Hamilton Rating Scale for Depression, and executive function, attention, working memory, and verbal fluency were assessed using a neuropsychological battery. Results: We included 46 (63.0%) men and 27 (36.9%) women, with mean ages of 55.2 (SD ± 15.1) and 46.8 (SD ± 14.7) years, respectively. We found significant improvement in the digit span forward and Stroop dots from month 1 to month 4 post stroke for both men and women. Women, but not men, presented a correlation between changes in phonemic verbal fluency and changes in the 31-item version of the Hamilton Rating Scale for Depression scores. Improvement in depression was correlated with improvement in verbal fluency, and worsening in depression was correlated with worsening in verbal fluency. Conclusions: Our results suggest that women might be more vulnerable to the relationship between depressive symptoms and cognitive performance, and improvement of depression may be necessary for women's improvement in phonemic verbal fluency from the first to the fourth month after a stroke. We did not adjust the results for multiple comparisons. Thus, our findings might be considered preliminary, and confirmatory studies, also focusing on specific characteristics of women that could explain these differences, are warranted.

There is limited evidence on fruit and vegetable intake in relation to cognitive function. This study aimed to evaluate the associations of quantity and variety in fruit and vegetable intake in midlife with cognitive impairment in late life. We used data from 16 737 participants of the Singapore Chinese Health Study, a population-based cohort study. The participants provided dietary data at recruitment at median age of 52·5 (range: 45-74) years and also participated in the third follow-up interview 20 years later at median age of 72·2 (range: 61-96) years. Quantity and variety of fruits and vegetables consumed at baseline were measured using a validated FFQ. Cognitive impairment at the third follow-up was defined using a Singapore-modified version of Mini-Mental State Examination. About 14·3 % participants had cognitive impairment. In multivariable logistic regression models, comparing extreme quartiles for intake of fruits and vegetables combined, the OR (95 % CI) associated with cognitive impairment was 0·83 (95 % CI: 0·73, 0·95; P-trend = 0·006) for quantity and 0·76 (95 % CI: 0·67, 0·87; P-trend< 0·001) for variety scores. Independently, those with increased variety of fruit intake or higher quantity of vegetable intake also had significantly 22 % and 15 % reduced odds of cognitive impairment, respectively. Finally, compared with those with low intake for both quantity and variety, those with both high quantity and variety for fruits and vegetables had 23 % reduction in odds of cognitive impairment. In conclusion, increase in quantity and variety of fruits and vegetables in midlife may reduce the risk of cognitive impairment in late life.

The prognostic value of temporal muscle mass has been studied in various neurological disorders. Herein, we investigated the association between temporal muscle mass and early cognitive function in patients with acute ischemic stroke. This study included 126 patients with acute cerebral infarction aged ≥65 years. Temporal muscle thickness (TMT) was measured using T2-weighted brain magnetic resonance imaging at admission for acute stroke. Within 2 weeks of stroke onset, skeletal mass index (SMI) and cognitive function were assessed using bioelectrical impedance analysis and the Korean version of the Montreal Cognitive Assessment (MoCA), respectively. Pearson's correlation analyzed the correlation between TMT and SMI, and multiple linear regression analyzed independent predictors of early post-stroke cognitive function. TMT and SMI were significantly positively correlated (R = 0.36, p < 0.001). After adjusting for covariates, TMT was an independent predictor of early post-stroke cognitive function, stratified by the MoCA score (β = 1.040, p = 0.017), age (β = -0.27, p = 0.006), stroke severity (β = -0.298, p = 0.007), and education level (β = 0.38, p = 0.008). TMT may be used as a surrogate marker for evaluating skeletal muscle mass because it is significantly associated with post-stroke cognitive function during the acute phase of ischemic stroke; therefore, TMT may help detect older patients at a high risk of early post-stroke cognitive impairment.

Background: Post-stroke cognitive impairment (PSCI) is a major complication of stroke that affects more than one-third of stroke survivors, threatening their quality of life and increasing the risk of disability and death. Although various studies have described the etiology, epidemiology, and risk factors of PSCI, there are a limited number of comprehensive and accurate reports on research trends and hotspots in this field. Therefore, this review aimed to evaluate research trends, hotspots, and frontiers in PSCI using bibliometric analysis. Methods: We screened the literature spanning 20 years in the Web of Science Core Collection: Science Citation Index Expanded (SCI-Expanded) database from 1 January 2003 to 31 December 2022. We included all eligible literature reports based on our comprehensive search strategy, inclusion criteria, and exclusion criteria. The analysis of annual publications, countries/regions, institutions, journals, co-cited references, and keywords was conducted using CiteSpace and VOSviewer, and the hotspots and major findings of PSCI were summarized. Results: A total of 1,024 publications were included in this review. We found that the number of publications on PSCI increased annually. These publications were published in 75 countries or regions by over 400 institutions. Although Chinese institutions had the highest number of publications, their international influence was limited. The United States showed a strong influence in the field. The journal "Stroke" published the most publications (57) with a high impact factor and was considered the most co-cited journal. The most frequently cited references focused on the prevalence, incidence, neuropsychological assessment scales, criteria, and guidelines of PSCI. The strongest citation burst keywords for PSCI were "neurotrophic factor" and "synaptic plasticity", which were regarded as research focuses and research hotspots, respectively. Conclusion: This review provided a comprehensive summary of the literature of PSCI, identified the authoritative and frequently cited literature and journals, clarified the trends in PSCI research, and highlighted the hotspots in this field. Currently, studies on the mechanisms and treatment of PSCI are limited, and we hope that this review has effectively highlighted the research trajectory of PSCI and will lay the foundation for more innovative research in the future.

Post-stroke cognitive impairment (PSCI) is a considerable risk factor for developing dementia and reoccurrence of stroke. Understanding the neural mechanisms of cognitive impairment after stroke can facilitate early identification and intervention.

Using functional near-infrared spectroscopy (fNRIS), the present study aimed to examine whether resting-state functional connectivity (FC) of brain networks differs in patients with PSCI, patients with Non-PSCI (NPSCI), and healthy controls (HCs), and whether these features could be used for clinical diagnosis of PSCI.

The present study recruited 16 HCs and 32 post-stroke patients. Based on the diagnostic criteria of PSCI, post-stroke patients were divided to the PSCI or NPSCI group. All participants underwent a 6-min resting-state fNRIS test to measure the hemodynamic responses from regions of interests (ROIs) that were primarily distributed in the prefrontal, somatosensory, and motor cortices.

The results showed that, when compared to the HC group, the PSCI group exhibited significantly decreased interhemispheric FC and intra-right hemispheric FC. ROI analyses showed significantly decreased FC among the regions of somatosensory cortex, dorsolateral prefrontal cortex, and medial prefrontal cortex for the PSCI group than for the HC group. However, no significant difference was found in the FC between the PSCI and the NPSCI groups.

Our findings provide evidence for compromised interhemispheric and intra-right hemispheric functional connectivity in patients with PSCI, suggesting that fNIRS is a promising approach to investigate the effects of stroke on functional connectivity of brain networks.

Post-stroke cognitive impairment, is a major complication of stroke, characterized by cognitive dysfunction, which directly affects the quality of life. Post-stroke cognitive impairment highlights the causal relationship between stroke and cognitive impairment. The pathological damage of stroke, including the increased release of excitatory amino acids, oxidative stress, inflammatory responses, apoptosis, changed neurotrophic factor levels and gene expression, influence synaptic plasticity. Synaptic plasticity refers to the activity-dependent changes in the strength of synaptic connections and efficiency of synaptic transmission at pre-existing synapses and can be divided into structural synaptic plasticity and functional synaptic plasticity. Changes in synaptic plasticity have been proven to play important roles in the occurrence and treatment of post-stroke cognitive impairment. Evidence has indicated that Chinese herbal drugs have effect of treating post-stroke cognitive impairment. In this review, we overview the influence of pathological damage of stroke on synaptic plasticity, analyze the changes of synaptic plasticity in post-stroke cognitive impairment, and summarize the commonly used Chinese herbal drugs whose active ingredient or extracts can regulate synaptic plasticity. This review will summarize the relationship between post-stroke cognitive impairment and synaptic plasticity, provide new ideas for future exploration of the mechanism of post-stroke cognitive impairment, compile evidence of applying Chinese herbal drugs to treat post-stroke cognitive impairment and lay a foundation for the development of novel formulas for treating post-stroke cognitive impairment.

Stroke is a debilitating disease that affects over 15 million people worldwide each year, resulting in the death of one-third of those people and severe disability in two-thirds of survivors. Previous studies reported various health benefits of Royal jelly in the context of its anti-inflammatory properties. We will aim to investigate the effects of royal jelly supplementation on oxidative stress, inflammatory mediators, mental health, cognitive function, quality of life, and clinical outcomes of patients with ischemic stroke.

The present study will be a triple-blind randomized placebo trial. Patients who meet our eligibility criteria will be assigned to the intervention or the control groups to receive allocated intervention for 12 weeks. Individuals of the intervention group will consume 1000 mg of Royal jelly dragee daily after breakfast. Subjects of the control group will receive a placebo dragee identical to the Royal jelly dragee. The severity of the stroke, cognitive function, mental health, quality of life, clinical outcomes, and biochemical measures will be assessed at baseline and post-intervention.

The current study is designed to investigate the effectiveness and safety of royal jelly supplementation in a randomized, parallel, two-arms, single-center, triple-blind, placebo-controlled manner. This study will provide evidence as a phase III clinical trial.

IRCT20180818040827N4, registered on 16 October 2021. https://www.irct.ir/trial/59275.