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Jones GH, Rong C, Shariq AS, Mishra A, Machado-Vieira R. Intracellular Signaling Cascades in Bipolar Disorder. Curr Top Behav Neurosci 2021; 48:101-132. [PMID: 32860212 DOI: 10.1007/7854_2020_157] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
Bipolar spectrum disorders carry a significant public health burden. Disproportionately high rates of suicide, incarceration, and comorbid medical conditions necessitate an extraordinary focus on understanding the intricacies of this disease. Elucidating granular, intracellular details seems to be a necessary preamble to advancing promising therapeutic opportunities. In this chapter, we review a wide range of intracellular mechanisms including mitochondrial energetics, calcium signaling, neuroinflammation, the microbiome, neurotransmitter metabolism, glycogen synthase kinase 3-beta (GSK3β), protein kinase C (PKC) and diacylglycerol (DAG), and neurotrophins (especially BDNF), as well as the glutamatergic, dopaminergic, purinergic, and neurohormonal systems. Owing to the relative lack of understanding and effective therapeutic options compared to the rest of the spectrum, special attention is paid in the chapter to the latest developments in bipolar depression. Likewise, from a therapeutic standpoint, special attention should be paid to the pervasive mechanistic actions of lithium as a means of amalgamating numerous, disparate cascades into a digestible cognitive topology.
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Affiliation(s)
- Gregory H Jones
- Department of Psychiatry, University of Texas Health Science Center at Houston, Houston, TX, USA
| | - Carola Rong
- Department of Psychiatry, University of Texas Health Science Center at Houston, Houston, TX, USA
| | - Aisha S Shariq
- Department of Psychiatry, Texas Tech University Health Science Center, El Paso, TX, USA
- Texas Tech University Health Science Center, Paul L. Foster School of Medicine, El Paso, TX, USA
| | - Abhinav Mishra
- Texas Tech University Health Science Center, Paul L. Foster School of Medicine, El Paso, TX, USA
| | - Rodrigo Machado-Vieira
- Department of Psychiatry, University of Texas Health Science Center at Houston, Houston, TX, USA.
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2
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Omranifard V, Tarrahi MJ, Sharifi S, Karahmadi M. Evaluation of the Effect of Memantine Supplementation in the Treatment of Acute Phase of Mania in Bipolar Disorder of Elderly Patients: A Double-blind Randomized Controlled Trial. Adv Biomed Res 2018; 7:148. [PMID: 30596058 PMCID: PMC6282487 DOI: 10.4103/abr.abr_110_18] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022] Open
Abstract
Background: This study aimed to evaluate the efficacy of memantine in the acute treatment of geriatric with bipolar disorder (BD) hospitalized for mania. Materials and Methods: This study conducted on 70 patients older than 60 years with BD in the acute phase of mania. Oral sodium valproate was prescribed in both groups. The intervention group received memantine tablet and the placebo group received a placebo tablet based on a same procedure. Severity of mania, cognitive changes, and quality of life (QoL) were assessed and recorded 4 and 8 weeks after the beginning of the study. The collected data were analyzed with SPSS (version 20) using independent samples t-test, analysis of variance in repeated observations, Chi-squared test, and Fisher's exact test. Results: Mania severity score had no significant difference at the beginning of the study, but 4 and 8 weeks after the intervention, it was reduced significantly in both groups (P < 0.001) that was higher in memantine group (P = 0.038). The mean increase in score of cognitive variations was 6.74 in the memantine group and 3.62 in the placebo group with a nonsignificant difference (P = 0.125). The scores of each dimension of QoL in the two groups showed that in all four dimensions, the patient's physical, psychological, social, and environmental status increased significantly by time (P < 0.001). Conclusions: According to the results of this study, memantine as an adjuvant to administration of sodium valproate may have a significant effect on decreasing the intensity of mania in the long run.
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Affiliation(s)
- Victoria Omranifard
- Department of Psychiatry, Isfahan University of Medical Sciences, Isfahan, Iran
| | - Mohammad Javad Tarrahi
- Department of Biostatistics and Epidemiology, Faculty of Health, Lorestan University of Medical Sciences, Khorramabad, Iran
| | - Shima Sharifi
- Department of Psychiatry, Isfahan University of Medical Sciences, Isfahan, Iran
| | - Mojgan Karahmadi
- Department of Psychiatry, School of Medicine, Isfahan University of Medical Sciences, Noor Hospital, Isfahan, Iran
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3
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Demontis F, Serra F, Serra G. Antidepressant-induced Dopamine Receptor Dysregulation: A Valid Animal Model of Manic-Depressive Illness. Curr Neuropharmacol 2018; 15:417-423. [PMID: 28503114 PMCID: PMC5405612 DOI: 10.2174/1570159x14666160715165648] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/10/2016] [Revised: 03/05/2016] [Accepted: 05/24/2016] [Indexed: 11/22/2022] Open
Abstract
Background: Mania seems to be associated with an increased dopamine (DA) transmission. Antidepressant treatments can induce mania in humans and potentiated DA transmission in animals, by sensitizing DA D2 receptors in the mesolimbic system. We have suggested that the sensitization of D2 receptors may be responsible of antidepressant-induced mania. This review aims to report the experimental evidence that led to the hypothesis that antidepressant-induced DA receptors dysregulation can be considered an animal model of bipolar disorder. Methods: We reviewed papers reporting preclinical and clinical studies on the role of DA in the mechanism of action of antidepressant treatments and in the patho-physiology of mood disorders. Results: A number of preclinical and clinical evidence suggests that mania could be associated with an increased DA activity, while a reduced function of this neurotransmission might underlie depression. Chronic treatment with imipramine induces a sensitization of DA D2 receptors in the mesolimbic system, followed, after drug discontinuation, by a reduced sensitivity associated with an increased immobility time in forced swimming test of depression (FST). Blockade of glutamate NMDA receptors by memantine administration prevents the imipramine effect on DA receptors sensitivity and on the FST. Conclusion: We suggest that chronic treatment with antidepressants induces a behavioural syndrome that mimics mania (the sensitization of DA receptors), followed by depression (desensitization of DA receptors and increased immobility time in the FST), i.e. an animal model of bipolar disorder. Moreover the observation that memantine prevents the “bipolar-like” behavior, suggests that the drug may have an antimanic and mood stabilizing effect. Preliminary clinical observations support this hypothesis.
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Affiliation(s)
- Francesca Demontis
- Department of Biomedical Sciences, University of Sassari, 07100 Sassari, Italy
| | - Francesca Serra
- Department of General Psychology, University of Padua, Italy
| | - Gino Serra
- Department of Biomedical Sciences, University of Sassari, 07100 Sassari, Italy
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Corrêa-Velloso JC, Gonçalves MC, Naaldijk Y, Oliveira-Giacomelli Á, Pillat MM, Ulrich H. Pathophysiology in the comorbidity of Bipolar Disorder and Alzheimer's Disease: pharmacological and stem cell approaches. Prog Neuropsychopharmacol Biol Psychiatry 2018; 80:34-53. [PMID: 28476640 DOI: 10.1016/j.pnpbp.2017.04.033] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/02/2017] [Accepted: 04/28/2017] [Indexed: 12/22/2022]
Abstract
Neuropsychiatric disorders involve various pathological mechanisms, resulting in neurodegeneration and brain atrophy. Neurodevelopmental processes have shown to be critical for the progression of those disorders, which are based on genetic and epigenetic mechanisms as well as on extrinsic factors. We review here common mechanisms underlying the comorbidity of Bipolar Disorders and Alzheimer's Disease, such as aberrant neurogenesis and neurotoxicity, reporting current therapeutic approaches. The understanding of these mechanisms precedes stem cell-based strategies as a new therapeutic possibility for treatment and prevention of Bipolar and Alzheimer's Disease progression. Taking into account the difficulty of studying the molecular basis of disease progression directly in patients, we also discuss the importance of stem cells for effective drug screening, modeling and treating psychiatric diseases, once in vitro differentiation of patient-induced pluripotent stem cells provides relevant information about embryonic origins, intracellular pathways and molecular mechanisms.
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Affiliation(s)
- Juliana C Corrêa-Velloso
- Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, SP 05508-000, Brazil
| | - Maria Cb Gonçalves
- Departamento de Neurologia e Neurociências, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Pedro de Toledo 669, São Paulo, SP 04039-032, Brazil
| | - Yahaira Naaldijk
- Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, SP 05508-000, Brazil
| | - Ágatha Oliveira-Giacomelli
- Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, SP 05508-000, Brazil
| | - Micheli M Pillat
- Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, SP 05508-000, Brazil
| | - Henning Ulrich
- Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, SP 05508-000, Brazil.
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5
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Duan J, Lao C, Chen J, Pan F, Zhang C, Xu W, Zhou W, Hu J, Shang D, Huang M, Xu Y. Memantine induces manic episode in a 73-year-old patient with vascular neurocognitive disorder: a case report. Neuropsychiatr Dis Treat 2018; 14:1395-1398. [PMID: 29881276 PMCID: PMC5985765 DOI: 10.2147/ndt.s160832] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022] Open
Abstract
Memantine, an N-methyl-d-aspartate receptor antagonist, is a well-established treatment option for moderate-to-severe cognitive impairment related to Alzheimer disease. Recently, growing evidence has indicated memantine might also be effective in treatment of affective disorders. The common drug-induced adverse events of memantine include confusion, dizziness, drowsiness, headache, insomnia, and agitation. Herein, we presented a case of a 73-year-old female patient with vascular neurocognitive disorder, who developed a manic episode after taking memantine.
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Affiliation(s)
- Jinfeng Duan
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Chengming Lao
- College of Medicine, Zhejiang University, Hangzhou, People's Republic of China.,Yiwu Mental Health Center, Yiwu, People's Republic of China
| | - Jingkai Chen
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Fen Pan
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Chenlin Zhang
- College of Medicine, Zhejiang University, Hangzhou, People's Republic of China
| | - Weijuan Xu
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Weihua Zhou
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Jianbo Hu
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Desheng Shang
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China
| | - Manli Huang
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
| | - Yi Xu
- Department of Psychiatry, First Affiliated Hospital, College of Medicine, Zhejiang University, The Key Laboratory of Mental Disorder's Management of Zhejiang Province, Hangzhou, People's Republic of China.,Brain Research Institute of Zhejiang University, Hangzhou, People's Republic of China
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6
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Demontis F, Serra G. Failure of memantine to “reverse” quinpirole-induced hypomotility. World J Psychiatry 2016; 6:215-220. [PMID: 27354963 PMCID: PMC4919260 DOI: 10.5498/wjp.v6.i2.215] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/12/2015] [Revised: 01/28/2016] [Accepted: 03/16/2016] [Indexed: 02/05/2023] Open
Abstract
AIM: To evaluate antidepressant-like effect of memantine in a rat model.
METHODS: Male Wistar rats were treated intraperitoneally with either vehicle, memantine (10 mg/kg) or imipramine (20 mg/kg), for 3 wk. Twenty-four hour after the last treatment animals were challenged with quinpirole (0.3 mg/kg s.c.) and tested for motor activity. After 1 h habituation to the motility cages, the motor response was recorded for the following 45-min and the data were collected in 5-min time bins.
RESULTS: As expected, chronic treatment with imipramine potentiated the locomotor stimulant effect of quinpirole. On the contrary, chronic memantine administration failed to induce the behavioral supersensitivity to the dopamine agonist.
CONCLUSION: The results show that memantine, at variance with antidepressant treatments, fails to induce dopaminergic behavioral supersensitivity. This observation is consistent with the results of preclinical and clinical studies suggesting that memantine does not have an acute antidepressant action but does have an antimanic and mood-stabilizing effect.
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7
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Acetylcholinesterase inhibitors and memantine in bipolar disorder: A systematic review and best evidence synthesis of the efficacy and safety for multiple disease dimensions. J Affect Disord 2016; 197:268-80. [PMID: 27010579 DOI: 10.1016/j.jad.2016.03.034] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/31/2015] [Revised: 02/09/2016] [Accepted: 03/09/2016] [Indexed: 12/17/2022]
Abstract
BACKGROUND Acetylcholinesterase inhibitors (AceI) and memantine might prove useful in bipolar disorder (BD) given their neuroprotective and pro-cognitive effects, as highlighted by several case reports. We aimed to systematically review the efficacy and safety of AceI and memantine across multiple outcome dimensions in BD. METHODS Systematic PubMed and SCOPUS search until 04/17/2015 without language restrictions. Included were randomized controlled trials (RCTs), open label studies and case series of AceI or memantine in BD patients reporting quantitative data on depression, mania, psychotic symptoms, global functioning, or cognitive performance. We summarized results using a best-evidence based synthesis. RESULTS Out of 214 hits, 12 studies (RCTs=5, other designs=7, total n=422) were included. Donepezil (studies=5; treated=102 vs. placebo=21): there was strong evidence for no effect on mania and psychotic symptoms; low evidence indicating no effect on depression. Galantamine (studies=3; treated=21 vs. controls=20) (placebo=10, healthy subjects=10): there was strong evidence for no effect on mania; moderate evidence for no effect on depression; low evidence for no effect on global functioning. Memantine (studies=4; treated=152 vs. placebo=88): there was conflicting evidence regarding efficacy for mania, depression and global functioning. LIMITATIONS Paucity of RCTs; small sample size studies; heterogeneous design, outcome and patient characteristics. CONCLUSION There is limited but converging evidence of no effect of AceI in BD, and conflicting evidence about memantine in BD. Too few studies of mostly medium/low quality and lacking sufficient numbers of patients in specific mood states, especially mania, contributed data, focusing solely on short-term/medium-term treatment, necessitating additional high-quality research to yield more definite results.
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Demontis F, Falconi M, Canu D, Serra G. Memantine prevents "bipolar-like" behavior induced by chronic treatment with imipramine in rats. Eur J Pharmacol 2015; 752:49-54. [PMID: 25661848 DOI: 10.1016/j.ejphar.2015.01.041] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2014] [Revised: 01/11/2015] [Accepted: 01/22/2015] [Indexed: 12/15/2022]
Abstract
A great deal of evidence suggests that virtually all antidepressant treatments induce a dopaminergic behavioral supersensitivity. We have suggested that this effect may play a key role not only in the antidepressant effect of these treatments, but also in their ability to induce a switch from depression to mania. In 2003-4 we found that the sensitization of dopamine receptors induced by imipramine is followed, after imipramine withdrawal, by a desensitization of these receptors associated with a depressive-like behavior assessed in the forced swimming test. The dopamine receptor sensitization can be prevented by MK-801, an NMDA receptor antagonist, but not by currently used mood stabilizers (lithium, carbamazepine, valproate). These observations led us to suggest - and later confirm - with preliminary clinical observations that memantine may have an acute antimanic and a long-lasting mood-stabilizing effect in treatment-resistant bipolar disorder patients. Here we present data showing that memantine prevents not only the dopamine receptor sensitization induced by imipramine, as observed with MK-801, but also the ensuing desensitization and the associated depressive-like behaviorq observed after antidepressant withdrawal.
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Affiliation(s)
| | - Marcella Falconi
- Dipartimento di Scienze Biomediche, Università di Sassari, Italy
| | - Desirèe Canu
- Dipartimento di Scienze Biomediche, Università di Sassari, Italy
| | - Gino Serra
- Dipartimento di Scienze Biomediche, Università di Sassari, Italy.
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9
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Serra G, Demontis F, Serra F, De Chiara L, Spoto A, Girardi P, Vidotto G, Serra G. Memantine: New prospective in bipolar disorder treatment. World J Psychiatry 2014; 4:80-90. [PMID: 25540723 PMCID: PMC4274590 DOI: 10.5498/wjp.v4.i4.80] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/28/2014] [Revised: 11/23/2014] [Accepted: 12/03/2014] [Indexed: 02/05/2023] Open
Abstract
UNLABELLED We review preclinical and clinical evidences strongly suggesting that memantine, an old drug currently approved for Alzheimer's dementia, is an effective treatment for acute mania and for the prevention of manic/hypomanic and depressive recurrences of manic-depressive illness. Lithium remains the first line for the treatment and prophylaxis of bipolar disorders, but currently available treatment alternatives for lithium resistant patients are of limited and/or questionable efficacy. Thus, research and development of more effective mood stabilizer drugs is a leading challenge for modern psychopharmacology. We have demonstrated that 21 d administration of imipramine causes a behavioural syndrome similar to a cycle of bipolar disorder, i.e., a mania followed by a depression, in rats. Indeed, such treatment causes a behavioural supersensitivity to dopamine D2 receptor agonists associated with an increase sexual activity and aggressivity (mania). The dopamine receptor sensitization is followed, after imipramine discontinuation, by an opposite phenomenon (dopamine receptor desensitization) and an increased immobility time (depression) in the forced swimming test of depression. Memantine blocks the development of the supersensitivity and the ensuing desensitization associated with the depressive like behavior. On the basis of these observations we have suggested the use of memantine in the treatment of mania and in the prophylaxis of bipolar disorders. To test this hypothesis we performed several naturalistic studies that showed an acute antimanic effect and a long-lasting and progressive mood-stabilizing action (at least 3 years), without clinically relevant side effects. To confirm the observations of our naturalistic trials we are now performing a randomized controlled clinical trial. Finally we described the studies reporting the efficacy of memantine in manic-like symptoms occurring in psychiatric disorders other than bipolar. LIMITATIONS A randomized controlled clinical trial is needed to confirm our naturalistic observations. CONCLUSION We believe that this review presents enough pharmacological and clinical information to consider the administration of memantine in the treatment of bipolar disorders that no respond to standard mood stabilizers.
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10
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Serra G, De Chiara L, Manfredi G, Koukopoulos AE, Sani G, Girardi P, Koukopoulos A, Serra G. Memantine in the management of affective recurrences of bipolar disorders after the discontinuation of long-term lithium treatment: three case histories. Ther Adv Psychopharmacol 2014; 4:53-5. [PMID: 24490033 PMCID: PMC3896132 DOI: 10.1177/2045125313507737] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/29/2022] Open
Affiliation(s)
- Giulia Serra
- NeSMOS Department (Neurosciences, Mental Health and Sensory Organs), School of Medicine and Psychology, Sapienza University, UOC Psychiatry, Sant'Andrea Hospital, Rome, Italy and Centro Lucio Bini, Rome, Italy
| | - Lavinia De Chiara
- NeSMOS Department (Neurosciences, Mental Health and Sensory Organs), School of Medicine and Psychology, Sapienza University, UOC Psychiatry, Sant'Andrea Hospital, Rome, Italy and Centro Lucio Bini, Rome, Italy
| | - Giovanni Manfredi
- NeSMOS Department (Neurosciences, Mental Health and Sensory Organs), School of Medicine and Psychology, Sapienza University, UOC Psychiatry, Sant'Andrea Hospital, Rome, Italy and Centro Lucio Bini, Rome, Italy
| | - Alexia E Koukopoulos
- NeSMOS Department (Neurosciences, Mental Health and Sensory Organs), School of Medicine and Psychology, Sapienza University, UOC Psychiatry, Sant'Andrea Hospital, Rome, Italy and Centro Lucio Bini, Rome, Italy
| | - Gabriele Sani
- NeSMOS Department (Neurosciences, Mental Health and Sensory Organs), School of Medicine and Psychology, Sapienza University, UOC Psychiatry, Sant'Andrea Hospital, Rome, Italy and Centro Lucio Bini, Rome, Italy and IRCCS Santa Lucia Foundation, Department of Clinical and Behavioural Neurology, Neuropsychiatry Laboratory, Rome, Italy
| | - Paolo Girardi
- NeSMOS Department (Neurosciences, Mental Health and Sensory Organs), School of Medicine and Psychology, Sapienza University, UOC Psychiatry, Sant'Andrea Hospital, Rome, Italy and Centro Lucio Bini, Rome, Italy and IRCCS Santa Lucia Foundation, Department of Clinical and Behavioural Neurology, Neuropsychiatry Laboratory, Rome, Italy
| | | | - Gino Serra
- Department of Biomedical Sciences, University of Sassari, Viale San Pietro, 43/b, 07100 Sassari Italy
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