• Alzheimer Disease
• Lgals3bp
• LysoIP
• Tmed5
• apoE4
• lysosomes
• pH

• R25 NS065723 NINDS NIH HHS
• U54 NS123746 NINDS NIH HHS
• R01 AG071697 NIA NIH HHS
• U24 NS072026 NINDS NIH HHS
• P30 AG019610 NIA NIH HHS
• RF1 AG059751 NIA NIH HHS
• P30 AG062422 NIA NIH HHS

• cell therapy
• interneuron
• synaptic inhibition
• traumatic brain injury
• vision

• R01 NS113516 NINDS NIH HHS
• R01 NS124855 NINDS NIH HHS
• R21 AG066496 NIA NIH HHS
• U01 DA054170 NIDA NIH HHS

• Brain cells
• Chimeric mouse model
• Differentiate
• Function
• Human induced pluripotent stem cell
• Integration

• Humans
• Induced Pluripotent Stem Cells/transplantation
• Induced Pluripotent Stem Cells/physiology
• Animals
• Brain/cytology
• Mice
• Cell Differentiation/physiology
• Chimera
• Disease Models, Animal
• Brain Diseases/therapy

• Apolipoprotein
• Cognition
• Fear conditioning
• Genotype
• Learning
• Morris water maze
• Novel location
• Novel object
• Rodent

• Animals
• Apolipoprotein E4/genetics
• Mice
• Cognitive Dysfunction/metabolism
• Cognitive Dysfunction/physiopathology
• Gene Knock-In Techniques
• Humans
• Mice, Transgenic
• Disease Models, Animal
• Apolipoprotein E3/genetics

• Alzheimer's disease
• Amyloid
• Hyperactivity
• Mild cognitive impairment
• Mitochondrial dysfunction
• Somatostatin
• Tau
• neurodegeneration
• oxidative stress
• synaptic loss

• Humans
• Alzheimer Disease/metabolism
• Amyloid beta-Peptides/metabolism
• Somatostatin/metabolism
• Neurons/metabolism
• Neurofibrillary Tangles/pathology

• regeneration and repair in the nervous system
• developmental neurogenesis

• Ganglionic Eminence
• Brain
• Cerebral Cortex
• Hippocampus
• Interneurons/physiology
• Median Eminence

• R01 NS071785 NINDS NIH HHS
• NIH/NINDS

• Animals
• Alzheimer Disease/pathology
• Apolipoprotein E4/genetics
• Apolipoprotein E4/metabolism
• Neurons/metabolism
• Neuroglia/metabolism
• Astrocytes/metabolism

• P01 AG073082 NIA NIH HHS
• R01 AG065540 NIA NIH HHS
• R01 AG071697 NIA NIH HHS
• RF1 AG076647 NIA NIH HHS

• Molecular neuroscience
• Neuroscience
• Transcriptomics

• U54 AG054345 NIA NIH HHS
• U54 AG054349 NIA NIH HHS

• Humans
• Neurodegenerative Diseases/drug therapy
• Neurodegenerative Diseases/metabolism
• Alzheimer Disease/drug therapy
• Synapses/metabolism
• Signal Transduction
• Neuronal Plasticity

• Parkinson’s disease
• brain organoids
• neural replacement
• tissue engineering

• R01 NS117757 NINDS NIH HHS
• R35 NS097370 NINDS NIH HHS
• R35NS116843 to H.S. NIH HHS
• R35NS097370 to G-l.M NIH HHS
• R01-NS117757 to DKC NIH HHS
• R01-NS127895 to DKC NIH HHS
• R01NS119472 to HIC NIH HHS
• R01 NS127895 NINDS NIH HHS
• R01 NS119472 NINDS NIH HHS
• R35 NS116843 NINDS NIH HHS

• Amyloid-β
• Fast-spiking interneurons
• Gamma oscillations
• Levetiracetam
• Prodromal
• hippocampus

• GABA
• blood vessels
• cytoskeleton
• interneurons
• migration
• neurodevelopmental disorders
• oligodendrocytes
• therapy

• Cerebral Cortex/physiology
• Neurogenesis
• Interneurons/physiology
• Cell Movement/physiology

• PJT-173284 CIHR

• Alzheimer’s disease
• Kinase
• Phosphorylation
• Protein-protein interaction
• Ubiquitylation

• Actins/metabolism
• Alzheimer Disease/metabolism
• Apolipoprotein E3/genetics
• Apolipoprotein E3/metabolism
• Apolipoprotein E4/genetics
• Apolipoprotein E4/metabolism
• Apolipoproteins E/genetics
• Apolipoproteins E/metabolism
• Phosphorylation
• Proteomics
• Animals
• Mice

• R35 GM118119 NIGMS NIH HHS
• RF1 AG059751 NIA NIH HHS
• Howard Hughes Medical Institute

• Aducanumab
• Alzheimer's disease
• Blood-brain barrier
• Immunotherapy
• Lecanemab

• ASD
• FMRP
• Fragile X Syndrome
• excitation/inhibition balance
• interneuronopathy
• interneurons

• AD11 transgenic mice
• Alzheimer’s disease
• KCC2 dysfunction
• NGF
• bumetanide treatment
• cation-chloride co-transporters
• depolarizing GABAA-mediated neurotransmission

• H2020 European Research Council
• European Research Council
• Deutsche Forschungsgemeinschaft
• Fondation Roger de Spoelberch
• Egerton University
• A5 and Z2
• German Excellence Cluster 925 SyNergy
• EU/Horizon2020

Aberrant increases in neuronal network excitability may contribute to cognitive deficits in Alzheimer's disease (AD). However, the mechanisms underlying hyperexcitability of neurons are not fully understood. Voltage‐gated sodium channels (VGSC or Nav), which are involved in the formation of excitable cell's action potential and can directly influence the excitability of neural networks, have been implicated in AD‐related abnormal neuronal hyperactivity and higher incidence of spontaneous non‐convulsive seizures. Here, we have shown that the reduction of VGSC α‐subunit Nav1.6 (by injecting adeno‐associated virus (AAV) with short hairpin RNA (shRNA) into the hippocampus) rescues cognitive impairments and attenuates synaptic deficits in APP/PS1 transgenic mice. Concurrently, amyloid plaques in the hippocampus and levels of soluble Aβ are significantly reduced. Interfering with Nav1.6 reduces the transcription level of β‐site APP‐cleaving enzyme 1 (BACE1), which is Aβ‐dependent. In the presence of Aβ oligomers, knockdown of Nav1.6 reduces intracellular calcium overload by suppressing reverse sodium–calcium exchange channel, consequently increasing inactive NFAT1 (the nuclear factor of activated T cells) levels and thus reducing BACE1 transcription. This mechanism leads to a reduction in the levels of Aβ in APP/PS1 transgenic mice, alleviates synaptic loss, improves learning and memory disorders in APP/PS1 mice after downregulating Nav1.6 in the hippocampus. Our study offers a new potential therapeutic strategy to counteract hippocampal hyperexcitability and subsequently rescue cognitive deficits in AD by selective blockade of Nav1.6 overexpression and/or hyperactivity.

• Alzheimer's disease
• BACE1
• NFAT1
• Nav1.6 sodium channel
• amyloid-β
• hyperexcitability

Alzheimer’s disease (AD) is one of the most complicated progressive neurodegenerative brain disorders, affecting millions of people around the world. Ageing remains one of the strongest risk factors associated with the disease and the increasing trend of the ageing population globally has significantly increased the pressure on healthcare systems worldwide. The pathogenesis of AD is being extensively investigated, yet several unknown key components remain. Therefore, we aimed to extract new knowledge from existing data. Ten gene expression datasets from different brain regions including the hippocampus, cerebellum, entorhinal, frontal and temporal cortices of 820 AD cases and 626 healthy controls were analyzed using the robust rank aggregation (RRA) method. Our results returned 1713 robust differentially expressed genes (DEGs) between five brain regions of AD cases and healthy controls. Subsequent analysis revealed pathways that were altered in each brain region, of which the GABAergic synapse pathway and the retrograde endocannabinoid signaling pathway were shared between all AD affected brain regions except the cerebellum, which is relatively less sensitive to the effects of AD. Furthermore, we obtained common robust DEGs between these two pathways and predicted three miRNAs as potential candidates targeting these genes; hsa-mir-17-5p, hsa-mir-106a-5p and hsa-mir-373-3p. Three transcription factors (TFs) were also identified as the potential upstream regulators of the robust DEGs; ELK-1, GATA1 and GATA2. Our results provide the foundation for further research investigating the role of these pathways in AD pathogenesis, and potential application of these miRNAs and TFs as therapeutic and diagnostic targets.

• Alzheimer’s disease
• GABAergic synapse pathway
• differentially expressed genes
• retrograde endocannabinoid signaling

• Alzheimer's disease
• cognitive deficit
• hippocampus
• neurogenesis
• pro‐neurogenic therapy

• Aged
• Alzheimer Disease
• Animals
• Cognition/physiology
• Hippocampus
• Humans
• Neurogenesis/physiology
• Neurons

• Natural Science Foundation of China

The mammalian hippocampal dentate gyrus is a niche for adult neurogenesis from neural stem cells. Newborn neurons integrate into existing neuronal networks, where they play a key role in hippocampal functions, including learning and memory. In the ageing brain, neurogenic capability progressively declines while in parallel increases the risk for developing Alzheimer's disease (AD), the main neurodegenerative disorder associated with memory loss. Numerous studies have investigated whether impaired adult neurogenesis contributes to memory decline in AD. Here, we review the literature on adult hippocampal neurogenesis (AHN) and AD by focusing on both human and mouse model studies. First, we describe key steps of AHN, report recent evidence of this phenomenon in humans, and describe the specific contribution of newborn neurons to memory, as evinced by animal studies. Next, we review articles investigating AHN in AD patients and critically examine the discrepancies among different studies over the last two decades. Also, we summarize researches investigating AHN in AD mouse models, and from these studies, we extrapolate the contribution of molecular factors linking AD-related changes to impaired neurogenesis. Lastly, we examine animal studies that link impaired neurogenesis to specific memory dysfunctions in AD and review treatments that have the potential to rescue memory capacities in AD by stimulating AHN.

• aerobic exercise
• functional connectivity
• hippocampus
• memory
• neuroimaging

• Israel Science Foundation

Apolipoprotein E (APOE) genotypes typically increase risk of amyloid-β deposition and onset of clinical Alzheimer’s disease (AD). However, cognitive assessments in APOE transgenic AD mice have resulted in discord.

Analysis of 31 peer-reviewed AD APOE mouse publications (n = 3,045 mice) uncovered aggregate trends between age, APOE genotype, gender, modulatory treatments, and cognition.

T-tests with Bonferroni correction (significance = p < 0.002) compared age-normalized Morris water maze (MWM) escape latencies in wild type (WT), APOE2 knock-in (KI2), APOE3 knock-in (KI3), APOE4 knock-in (KI4), and APOE knock-out (KO) mice. Positive treatments (t+) to favorably modulate APOE to improve cognition, negative treatments (t–) to perturb etiology and diminish cognition, and untreated (t0) mice were compared. Machine learning with random forest modeling predicted MWM escape latency performance based on 12 features: mouse genotype (WT, KI2, KI3, KI4, KO), modulatory treatment (t+, t–, t0), mouse age, and mouse gender (male = g_m; female = g_f, mixed gender = g_mi).

KI3 mice performed significantly better in MWM, but KI4 and KO performed significantly worse than WT. KI2 performed similarly to WT. KI4 performed significantly worse compared to every other genotype. Positive treatments significantly improved cognition in WT, KI4, and KO compared to untreated. Interestingly, negative treatments in KI4 also significantly improved mean MWM escape latency. Random forest modeling resulted in the following feature importance for predicting superior MWM performance: [KI3, age, g_m, KI4, t0, t+, KO, WT, g_mi, t–, g_f, KI2] = [0.270, 0.094, 0.092, 0.088, 0.077, 0.074, 0.069, 0.061, 0.058, 0.054, 0.038, 0.023].

APOE3, age, and male gender was most important for predicting superior mouse cognitive performance.

• APOE
• Age
• Alzheimer’s disease
• Morris water maze
• cognitive function
• gender
• treatment

• Aging
• Alzheimer’s disease
• Episodic memory
• Hippocampus
• γ-aminobutyric acid

• Alzheimer Disease/genetics
• Animals
• Disease Models, Animal
• GABAergic Neurons/pathology
• Humans
• Memory Disorders/genetics
• Mice
• Neural Networks, Computer

• R00 AG055684 NIA NIH HHS

Adult hippocampal neurogenesis (AHN) is restricted under the pathological conditions of neurodegenerative diseases, especially in Alzheimer’s disease (AD). The drop of AHN reduces neural circuit plasticity, resulting in the decrease of the generation of newborn neurons in dentate gyrus (DG), which makes it difficult to recover from learning/memory dysfunction in AD, therefore, it is imperative to find a therapeutic strategy to promote neurogenesis and clarify its underlying mechanism involved.

Amyloid precursor protein/presenilin 1 (APP/PS1) mice were treated with photobiomodulation therapy (PBMT) for 0.1 mW/mm² per day in the dark for 1 month (10 min for each day). The neural stem cells (NSCs) were isolated from hippocampus of APP/PS1 transgenic mice at E14, and the cells were treated with PBMT for 0.667 mW/mm² in the dark (5 min for each time).

In this study, photobiomodulation therapy (PBMT) is found to promote AHN in APP/PS1 mice. The latent transforming growth factor-β1 (LTGFβ1) was activated in vitro and in vivo during PBMT-induced AHN, which promoted the differentiation of hippocampal APP/PS1 NSCs into newborn neurons. In particular, behavioral experiments showed that PBMT enhanced the spatial learning/memory ability of APP/PS1 mice. Mechanistically, PBMT-stimulated reactive oxygen species (ROS) activates TGFβ/Smad signaling pathway to increase the interaction of the transcription factors Smad2/3 with Smad4 and competitively reduce the association of Smad1/5/9 with Smad4, thereby significantly upregulating the expression of doublecortin (Dcx)/neuronal class-III β-tubulin (Tuj1) and downregulating the expression of glial fibrillary acidic protein (GFAP). These in vitro effects were abrogated when eliminating ROS. Furthermore, specific inhibition of TGFβ receptor I (TGFβR I) attenuates the DNA-binding efficiency of Smad2/3 to the Dcx promotor triggered by PBMT.

Our study demonstrates that PBMT, as a viable therapeutic strategy, directs the adult hippocampal APP/PS1 NSCs differentiate towards neurons, which has great potential value for ameliorating the drop of AHN in Alzheimer’s disease mice.

The online version contains supplementary material available at 10.1186/s13287-021-02399-2.

• Adult hippocampal neurogenesis
• Alzheimer’s disease model
• Neural stem cell
• Newborn neuron
• Photobiomodulation therapy
• Spatial learning/memory ability
• TGFβ/Smad pathway

A distinctive feature of the hippocampal structure is the diversity of inhibitory interneurons. These complex inhibitory interconnections largely contribute to the tight modulation of hippocampal circuitry, as well as to the formation and coordination of neuronal assemblies underlying learning and memory. Inhibitory interneurons provide more than a simple transitory inhibition of hippocampal principal cells (PCs). The synaptic plasticity of inhibitory neurons provides long-lasting changes in the hippocampal network and is a key component of memory formation. The dendrite targeting interneurons expressing the peptide somatostatin (SOM) are particularly interesting in this regard because they display unique long-lasting synaptic changes leading to metaplastic regulation of hippocampal networks. In this article, we examine the actions of the neuropeptide SOM on hippocampal cells, synaptic plasticity, learning, and memory. We address the different subtypes of hippocampal SOM interneurons. We describe the long-term synaptic plasticity that takes place at the excitatory synapses of SOM interneurons, its singular induction and expression mechanisms, as well as the consequences of these changes on the hippocampal network, learning, and memory. We also review evidence that astrocytes provide cell-specific dynamic regulation of inhibition of PC dendrites by SOM interneurons. Finally, we cover how, in mouse models of Alzheimer’s disease (AD), dysfunction of plasticity of SOM interneuron excitatory synapses may also contribute to cognitive impairments in brain disorders.

• Alzheimer’s disease
• hippocampus
• inhibitory interneuron
• long-term potentiation
• memory impairment
• network metaplasticity
• somatostatin
• spatial and contextual memory

• Alzheimer’s disease
• GABA
• cell transplantation
• hyperexcitability
• interneuron
• interneuron progenitor

• Alzheimer's disease
• ApoE4
• Neuronal activity
• Neuronal information coding
• Taste learning

Alzheimer’s disease (AD) is the most frequent neurodegenerative disorder that commonly causes dementia in the elderly. Recent evidence indicates that network abnormalities, including hypersynchrony, altered oscillatory rhythmic activity, interneuron dysfunction, and synaptic depression, may be key mediators of cognitive decline in AD. In this review, we discuss characteristics of neuronal network excitability in AD, and the role of Aβ and tau in the induction of network hyperexcitability. Many patients harboring genetic mutations that lead to increased Aβ production suffer from seizures and epilepsy before the development of plaques. Similarly, pathologic accumulation of hyperphosphorylated tau has been associated with hyperexcitability in the hippocampus. We present common and divergent roles of tau and Aβ on neuronal hyperexcitability in AD, and hypotheses that could serve as a template for future experiments.

• amyloid β
• neuronal excitability
• seizures
• tau

• GABA
• development
• hippocampus
• interneuron
• porcine

• Alzheimer’s disease
• epilepsy
• hyperexcitability
• neurodegeneration

• Alzheimer Disease/drug therapy
• Alzheimer Disease/metabolism
• Alzheimer Disease/physiopathology
• Animals
• Anticonvulsants/pharmacology
• Anticonvulsants/therapeutic use
• Brain/drug effects
• Brain/metabolism
• Brain/physiopathology
• Epilepsy/metabolism
• Epilepsy/physiopathology
• Humans
• Nootropic Agents/pharmacology
• Nootropic Agents/therapeutic use

• 206330/Z/17/Z Wellcome Trust

In this review, we present evidence about the changes of the GABAergic system on the hippocampus under the ischemic environment, which may be an underlying mechanism to the ischemia-induced cognitive deficit. GABAergic system, in contrast to the glutamatergic system, is considered to play an inhibitory effect on the central nervous system over the past several decades. It has received widespread attention in the area of schizophrenia and epilepsy. The GABAergic system has a significant effect in promoting neural development and formation of local neural circuits of the brain, which is the structural basis of cognitive function. There have been a number of reviews describing changes in the GABAergic system in cerebral ischemia in recent years. However, no study has investigated the changes in the system in the hippocampus during cerebral ischemic injury, which results in cognitive impairment, particularly at the chronic ischemic stage and the late phase of ischemia. We present a review of the changes of the GABAergic system in the hippocampus under ischemia, including GABA interneurons, extracellular GABA neurotransmitter, and GABA receptors. Several studies are also listed correlating amelioration of cognitive impairment by regulating the GABAergic system in the hippocampus damaged under ischemia. Furthermore, exogenous cell transplantation, which improves cognition by modulating the GABAergic system, will also be described in this review to bring new insight and strategy on solving cognitive deficits caused by cerebral ischemia.

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized clinically by severe cognitive deficits and pathologically by amyloid plaques, neuronal loss, and neurofibrillary tangles. Abnormal amyloid β-protein (Aβ) deposition in the brain is often thought of as a major initiating factor in AD neuropathology. However, gamma-aminobutyric acid (GABA) inhibitory interneurons are resistant to Aβ deposition, and Aβ decreases synaptic glutamatergic transmission to decrease neural network activity. Furthermore, there is now evidence suggesting that neural network activity is aberrantly increased in AD patients and animal models due to functional deficits in and decreased activity of GABA inhibitory interneurons, contributing to cognitive deficits. Here we describe the roles played by excitatory neurons and GABA inhibitory interneurons in Aβ-induced cognitive deficits and how altered GABA interneurons regulate AD neuropathology. We also comprehensively review recent studies on how GABA interneurons and GABA receptors can be exploited for therapeutic benefit. GABA interneurons are an emerging therapeutic target in AD, with further clinical trials urgently warranted.

• Alzheimer’s disease
• GABA inhibitory interneurons
• PV inhibitory interneurons
• amyloid β-protein
• cognitive deficits

• Alzheimer's disease
• E/I balance
• GABA
• GABA receptor
• GABAergic neuron
• amyloid β peptide

Accumulation of amyloid β oligomers (AβO) in Alzheimer’s disease (AD) impairs hippocampal theta and gamma oscillations. These oscillations are important in memory functions and depend on distinct subtypes of hippocampal interneurons such as somatostatin-positive (SST) and parvalbumin-positive (PV) interneurons. Here, we investigated whether AβO causes dysfunctions in SST and PV interneurons by optogenetically manipulating them during theta and gamma oscillations in vivo in AβO-injected SST-Cre or PV-Cre mice. Hippocampal in vivo multi-electrode recordings revealed that optogenetic activation of channelrhodopsin-2 (ChR2)-expressing SST and PV interneurons in AβO-injected mice selectively restored AβO-induced reduction of the peak power of theta and gamma oscillations, respectively, and resynchronized CA1 pyramidal cell (PC) spikes. Moreover, SST and PV interneuron spike phases were resynchronized relative to theta and gamma oscillations, respectively. Whole-cell voltage-clamp recordings in CA1 PC in ex vivo hippocampal slices from AβO-injected mice revealed that optogenetic activation of SST and PV interneurons enhanced spontaneous inhibitory postsynaptic currents (IPSCs) selectively at theta and gamma frequencies, respectively. Furthermore, analyses of the stimulus–response curve, paired-pulse ratio, and short-term plasticity of SST and PV interneuron-evoked IPSCs ex vivo showed that AβO increased the initial GABA release probability to depress SST/PV interneuron’s inhibitory input to CA1 PC selectively at theta and gamma frequencies, respectively. Our results reveal frequency-specific and interneuron subtype-specific presynaptic dysfunctions of SST and PV interneurons’ input to CA1 PC as the synaptic mechanisms underlying AβO-induced impairments of hippocampal network oscillations and identify them as potential therapeutic targets for restoring hippocampal network oscillations in early AD.

• Alzheimer's disease
• Amyloid beta oligomers
• Hippocampus
• Network oscillations
• Parvalbumin interneuron
• Somatostatin interneuron

• D4 receptor
• cognitive impairment
• parvalbumin
• sepsis
• γ oscillation

• Animals
• Cognitive Dysfunction/etiology
• Cognitive Dysfunction/metabolism
• Gamma Rhythm/physiology
• Hippocampus/metabolism
• Interneurons/metabolism
• Male
• Parvalbumins/metabolism
• Rats
• Rats, Sprague-Dawley
• Receptors, Dopamine D4/metabolism
• Sepsis/complications
• Sepsis/metabolism

• GABA
• GABAergic interneuron
• adult hippocampal neurogenesis
• astrogliosis
• cognitive impairment
• network hyperactivation
• tau accumulation

• brain stimulation
• excitatory/inhibitory balance
• therapeutic development

• Aged
• Alzheimer Disease/therapy
• Brain/physiology
• Humans
• Transcranial Magnetic Stimulation

• Apolipoprotein E
• basolateral amygdala
• conditioned taste aversion
• extinction
• gustatory cortex
• hippocampus
• learning
• medial prefrontal cortex
• synaptic plasticity
• synaptophysin
• taste
• vesicular GABA transporter
• vesicular glutamate transporter
• young age

Alzheimer’s disease (AD) is still a major public health challenge without an effective treatment to prevent or stop it. Routinely used acetylcholinesterase inhibitors and memantine seem to slow disease progression only to a limited extend. Therefore, many investigations on new drugs and other treatment modalities are ongoing in close association with increasing knowledge of the pathophysiology of the disease. Here, we review the studies about the new treatment modalities in AD with a classification based on their main targets, specifically pathologic structures of the disease, amyloid and tau, neural network dysfunction with special interest to the regulation of gamma oscillations, and attempts for the restoration of neural tissue via regenerative medicine. Additionally, we describe the evolving modalities related to gut microbiota, modulation, microglial function, and glucose metabolism.

• Alzheimer’s disease treatment
• Anti-amyloid
• Anti-tau
• Gamma oscillations
• Stem cell therapy

• Alzheimer’s disease
• Apolipoprotein E
• GABAergic interneuron
• Hyperexcitability
• Inhibitory network
• Selective vulnerability
• Tau

• Alzheimer Disease/genetics
• Alzheimer Disease/metabolism
• Animals
• Apolipoprotein E4/genetics
• Humans
• Induced Pluripotent Stem Cells/metabolism
• Memory/physiology
• Memory Disorders/genetics
• Memory Disorders/metabolism
• Nerve Net/metabolism

• RF1 AG055421 NIA NIH HHS
• RF1 AG047655 NIA NIH HHS
• R01 AG055682 NIA NIH HHS
• RF1 AG048030 NIA NIH HHS
• F31 AG057150 NIA NIH HHS
• National Institute on Aging

• Alzheimer’s disease
• Neurodegenerative disorders
• Stem cell therapy