Progress in Neuro-Psychopharmacology & Biological Psychiatry最新文献_第3页

Emotional dysregulation following prenatal stress is associated with altered prefrontal cortex responsiveness to an acute challenge in adolescence 产前应激后的情绪失调与青春期前额叶皮层对急性挑战的反应能力改变有关。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-09 DOI: 10.1016/j.pnpbp.2024.111162

{"title":"Emotional dysregulation following prenatal stress is associated with altered prefrontal cortex responsiveness to an acute challenge in adolescence","authors":"","doi":"10.1016/j.pnpbp.2024.111162","DOIUrl":"10.1016/j.pnpbp.2024.111162","url":null,"abstract":"<div><div>Exposure to prenatal stress (PNS) has the potential to elicit multiple neurobiological alterations and increase the susceptibility to psychiatric disorders. Moreover, gestational stress may sensitize the brain toward an altered response to subsequent challenges. Here, we investigated the effects of PNS in rats and assessed whether these animals exhibit an altered brain responsiveness to an acute stress (AS) during adolescence. From gestational day 14 until delivery, Sprague Dawley dams were exposed to PNS or left undisturbed. During adolescence (PND38 to PND41), offspring were tested in the social interaction and splash test. At PND44 half of the animals were exposed to 5 min of forced swim stress. Males and Females exposed to PNS showed reduced sociability and increased anhedonic-like behavior. At the molecular level, exposure of adolescent rats to AS produced increased activation of the amygdala and ventral and dorsal hippocampus. Regarding the prefrontal cortex (PFC), we observed a pronounced activation in PNS males exposed to AS. Cell-type specific transcriptional analyses revealed a significant imbalance in the activation of PFC excitatory and inhibitory neurons in PNS males and females exposed to AS. Furthermore, stressed males exhibited disrupted HPA-axis function, while females showed impairments in the modulation of antioxidant genes. Our study shows that PNS induces emotional dysregulation and alters the responsiveness of the PFC to an acute stressor. Moreover, the disruption of excitatory and inhibitory balance during adolescence could influence the ability to respond to challenging events that may contribute to precipitate a full-blown pathologic condition.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Associations between cytokine levels and cognitive function among individuals at clinical high risk for psychosis 精神病临床高危人群中细胞因子水平与认知功能之间的关系。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-09 DOI: 10.1016/j.pnpbp.2024.111166

{"title":"Associations between cytokine levels and cognitive function among individuals at clinical high risk for psychosis","authors":"","doi":"10.1016/j.pnpbp.2024.111166","DOIUrl":"10.1016/j.pnpbp.2024.111166","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the intricate interplay among cytokines, cognitive functioning, and conversion to psychosis in individuals at clinical high-risk (CHR) for psychosis.</div></div><div><h3>Method</h3><div>We initially enrolled 385 individuals at CHR and 95 healthy controls (HCs). Subsequently, 102 participants at CHR completed the 1-year follow-up assessments, and 47 participants transitioned to psychosis. We assessed the levels of interleukins (IL-1β, IL-2, IL-6, IL-8, IL-10), tumor necrosis factor-α (TNF-α), granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF). We comprehensively evaluated cognitive performance across six domains, including speed of processing (SP), attention/vigilance (AV), working memory (WM), verbal learning (VeL), visual learning (ViL), and reasoning and problem-solving (RPS).</div></div><div><h3>Results</h3><div>Higher baseline cognitive domain scores were associated with elevated GM-CSF and reduced VEGF levels. In the follow-up analysis, significant time effects were observed for IL-1β and IL-2. We also observed significant interaction effects between specific cognitive domains (AV, WM, VeL, and OCS) and levels of cytokine (GM-CSF, IL-1β, IL-6, and TNF-α). Changes in WM were negatively correlated with changes in TNF-α levels and positively correlated with changes in VEGF levels. Variations in VeL were inversely correlated with changes in GM-CSF and IL-10 levels, whereas changes in RPS were positively associated with changes in GM-CSF and IL-8 levels.</div></div><div><h3>Conclusions</h3><div>Our results revealed intricate associations among cytokine levels, cognitive performance, and psychosis progression.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identifying genetic variants associated with side effects of antidepressant treatment: A systematic review 确定与抗抑郁治疗副作用相关的基因变异：系统综述。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-05 DOI: 10.1016/j.pnpbp.2024.111154

{"title":"Identifying genetic variants associated with side effects of antidepressant treatment: A systematic review","authors":"","doi":"10.1016/j.pnpbp.2024.111154","DOIUrl":"10.1016/j.pnpbp.2024.111154","url":null,"abstract":"<div><div>Major Depressive Disorder (MDD) is one of the most prevalent neurobiological disorders globally. Antidepressant medications are the first-line treatment for managing symptoms. However, over time, pharmacotherapy has been linked to several challenges, primarily due to the wide array of side effects that often reduce patient adherence to treatment. The literature suggests that these side effects may be influenced by polymorphisms in genes related to the pharmacokinetics and pharmacodynamics of antidepressants. Thus, this systematic review aimed to identify studies that investigated the association between genetic variants and side effects resulting from antidepressant treatment in individuals with MDD. Original articles indexed in the electronic databases Cochrane Library, EMBASE, MEDLINE via PubMed, and Scopus were identified. A total of 55 studies were included in the review, and data regarding the outcomes of interest were extracted. Due to the exploratory nature of the review, a narrative/descriptive synthesis of the results was performed. The risk of bias was evaluated using the Joanna Briggs Institute's tools, tailored to the design of each study. Polymorphisms in 35 genes were statistically associated with the development of side effects. A subsequent Protein-Protein Interaction Network analysis helped elucidate the key biological pathways involved in antidepressant side effects, with a view toward exploring the potential application of pharmacogenetic markers in clinical practice.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antidepressants account for the causal effect of major depressive disorder on type 2 diabetes 抗抑郁药是重度抑郁症对 2 型糖尿病的因果效应。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-05 DOI: 10.1016/j.pnpbp.2024.111164

{"title":"Antidepressants account for the causal effect of major depressive disorder on type 2 diabetes","authors":"","doi":"10.1016/j.pnpbp.2024.111164","DOIUrl":"10.1016/j.pnpbp.2024.111164","url":null,"abstract":"<div><h3>Background</h3><div>Patients with major depressive disorder (MDD) face an elevated risk of type 2 diabetes (T2D). However, the contribution of the disease itself versus the side effects of antidepressants to this increased risk remains unclear.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the overall and independent effects of MDD and exposure to antidepressants on T2D risk.</div></div><div><h3>Methods</h3><div>Summary genome-wide association study datasets were utilized for the Mendelian randomization (MR) and multivariable MR (MVMR) analyses, including ones for MDD (<em>N</em> = 500,199), antidepressants (<em>N</em> = 175,161), and T2D (<em>N</em> = 933,970). Bayesian colocalization analysis was used to reveal shared genetic variation between MDD, antidepressants, and T2D.</div></div><div><h3>Results</h3><div>We found that both MDD (OR: 1.15, CI: 1.03–1.30, <em>P</em> = 0.016) and antidepressants (OR: 1.37, CI: 1.22–1.53, <em>P</em> = 2.75E-08) have overall causal effects on T2D. While T2D was associated with the risk of antidepressant use (OR: 1.08, CI: 1.06–1.11, <em>P</em> = 8.80E-10), but not with the risk of MDD (OR: 1.00, CI: 0.98–1.01, <em>P</em> = 0.661). Our MVMR analysis showed that the use of antidepressants is associated with higher risks of T2D (OR: 1.21, CI: 1.07–1.37, <em>P</em> = 7.19E-04), while MDD is not linked to the risk of T2D (OR: 1.01, CI: 0.86–1.18, <em>P</em> = 0.799). Colocalization analysis identified two shared genetic loci between antidepressants and T2D.</div></div><div><h3>Conclusions</h3><div>The elevated T2D risk in MDD patients is chiefly caused by antidepressant use. These findings emphasize the importance of considering the impact of antidepressants on metabolic health in individuals with MDD.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Allopregnanolone and intrusive memories: A potential therapeutic target for PTSD treatment? 异丙孕酮和侵入性记忆：创伤后应激障碍治疗的潜在治疗靶点？

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-05 DOI: 10.1016/j.pnpbp.2024.111168

引用次数: 0

Sex-specific association between schizophrenia polygenic risk and subclinical schizophrenia-related traits 精神分裂症多基因风险与亚临床精神分裂症相关特征之间的性别特异性关联。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-04 DOI: 10.1016/j.pnpbp.2024.111161

{"title":"Sex-specific association between schizophrenia polygenic risk and subclinical schizophrenia-related traits","authors":"","doi":"10.1016/j.pnpbp.2024.111161","DOIUrl":"10.1016/j.pnpbp.2024.111161","url":null,"abstract":"<div><h3>Background</h3><div>According to the dimensional view of psychiatric disorders, psychosis is expressed as a continuum in the general population. However, the investigation of the putative genetic aetiological continuity between its clinical and subclinical phenotypes has yielded mixed results. We aimed to replicate previous findings regarding the association of polygenic risk for schizophrenia with subclinical traits (i.e., schizotypy traits and psychotic-like experiences), and to examine the role of sex in this association in a large nonclinical sample.</div></div><div><h3>Methods</h3><div>The Multidimensional Schizotypy Scale and the Community Assessment of Psychic Experiences were assessed in 919 nonclinical participants. Polygenic Risk Scores for schizophrenia (SZ-PRSs) were computed using the PRS-CS method based on the latest genome-wide association study of schizophrenia. Summary statistics derived from the total GWAS sample and stratified by sex were used. Linear regression analyses tested the associations of the SZ-PRSs with the psychometric variables, both in the total sample and by sex.</div></div><div><h3>Results</h3><div>No associations were found between the SZ-PRSs and the positive, negative or disorganized dimensions of schizotypy in the total sample. Likewise, no associations were found with psychotic-like experiences. However, the sex-stratified analyses revealed a male-specific association with positive schizotypy. Similar results were obtained with the PRSs derived from the sex-stratified summary statistics.</div></div><div><h3>Discussion</h3><div>Our results are consistent with the lack of clear evidence of an association between SZ common genetic risk and its subclinical phenotypes. Nevertheless, the male-specific association found suggests that this PRS might explain better the male phenotype, as reported in previous studies. Future studies should put a focus on the role of sex in this association to unravel its sex specificities.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aberrant individual large-scale functional network connectivity and topology in chronic insomnia disorder with and without depression 伴有或不伴有抑郁症的慢性失眠症患者个体大规模功能网络连接和拓扑结构异常。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-03 DOI: 10.1016/j.pnpbp.2024.111158

{"title":"Aberrant individual large-scale functional network connectivity and topology in chronic insomnia disorder with and without depression","authors":"","doi":"10.1016/j.pnpbp.2024.111158","DOIUrl":"10.1016/j.pnpbp.2024.111158","url":null,"abstract":"<div><div>Insomnia is increasingly prevalent with significant associations with depression. Delineating specific neural circuits for chronic insomnia disorder (CID) with and without depressive symptoms is fundamental to develop precision diagnosis and treatment. In this study, we examine static, dynamic and network topology changes of individual large-scale functional network for CID with (CID-D) and without depression to reveal their specific neural underpinnings. Seventeen individual-specific functional brain networks are obtained using a regularized nonnegative matrix factorization technique. Disorders-shared and -specific differences in static and dynamic large-scale functional network connectivities within or between the cognitive control network, dorsal attention network, visual network, limbic network, and default mode network are found for CID and CID-D. Additionally, CID and CID-D groups showed compromised network topological architecture including reduced small-world properties, clustering coefficients and modularity indicating decreased network efficiency and impaired functional segregation. Moreover, the altered neuroimaging indices show significant associations with clinical manifestations and could serve as effective neuromarkers to distinguish among healthy controls, CID and CID-D. Taken together, these findings provide novel insights into the neural basis of CID and CID-D, which may facilitate developing new diagnostic and therapeutic approaches.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DNA methylation of serotonin genes as predictive biomarkers of antidepressant treatment response 血清素基因的 DNA 甲基化作为抗抑郁治疗反应的预测性生物标志物。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-03 DOI: 10.1016/j.pnpbp.2024.111160

{"title":"DNA methylation of serotonin genes as predictive biomarkers of antidepressant treatment response","authors":"","doi":"10.1016/j.pnpbp.2024.111160","DOIUrl":"10.1016/j.pnpbp.2024.111160","url":null,"abstract":"<div><div>Selective serotonin reuptake inhibitors (SSRI) are frequently ineffective in treating depressive episodes and biomarkers are needed to optimize antidepressant treatment outcomes. DNA methylation levels of serotonin transporter (<em>SLC6A4</em>) and tryptophan hydroxylase 2 genes (<em>TPH2</em>) have been suggested to predict antidepressant clinical outcomes but their applicability remains uncertain. In this study, we: 1) evaluated <em>SLC6A4</em>/<em>TPH2</em> methylation biomarker potential for predicting clinical outcomes after escitalopram treatment; 2) evaluated whether changes in <em>SLC6A4</em>/<em>TPH2</em> methylation are informative of treatment mechanisms. We used a cohort of 90 unmedicated patients with major depressive disorder that were part of a 12-week open-label longitudinal trial and compared our observations with previous findings. Depressive symptoms were measured at baseline and after 8 and 12 weeks of treatment using the Hamilton Depression Rating Scale (HAMD<sub>6/17</sub>). We found an association between baseline <em>TPH2</em> methylation and both clinical response (<em>β</em>:3.43; <em>p</em> = 0.01; 95 % CI:[0.80; 6.06]) and change in depressive symptoms after 8 weeks (<em>β</em>:−45.44; p = 0.01; 95 %CI:[− −78.58; −12.30]). However, we found no evidence for predictive value of any gene (<em>TPH2</em> AUC: 0.74 95 % CI:[0.42;0.79]; <em>SLC6A4</em>: AUC: 0.61; 95 % CI: [0.48–0.78]). Methylation levels changed at the trend level for CpG sites of <em>SLC6A4</em> and <em>TPH2</em> over the course of 12 weeks of treatment. In addition, similar to previous observations, we found a trend for an association between methylation of <em>SLC6A4</em> CpG2 (chr17:30,236,083) and HAMD<sub>17</sub> change after 12 weeks. Our findings suggest that although <em>TPH2</em> and <em>SLC6A4</em> methylation may be informative of antidepressant treatment outcome, they are unlikely to prove useful as clinical predictor tools.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Brain structural differences in cocaine use disorder: Insights from multivariate and neurotransmitter analyses 可卡因使用障碍的大脑结构差异：多变量和神经递质分析的启示。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-10-02 DOI: 10.1016/j.pnpbp.2024.111159

{"title":"Brain structural differences in cocaine use disorder: Insights from multivariate and neurotransmitter analyses","authors":"","doi":"10.1016/j.pnpbp.2024.111159","DOIUrl":"10.1016/j.pnpbp.2024.111159","url":null,"abstract":"<div><div>Cocaine use disorder (CUD) is a chronic and relapsing neuropsychiatric disorder characterized by structural and functional brain lesions, posing a significant public health challenge. While the disruptive effects of cocaine on neurotransmitter systems (receptors/transporters) have been well established, the patterns of brain structural abnormalities in CUD and its interaction with other factors remain an ongoing topic of investigation. We employed source-based morphometry (SBM), a multivariate approach on 50 CUD participants and 50 matched healthy controls from the public SUDMEX CONN dataset. This method allowed us to identify co-varying patterns of brain tissue volume differences, and further explore the effect of average cocaine dosage through moderation analysis. Spatial correlation analysis was also performed to examine micro-macro structural consistency between tissue volume variations and chemoarchitectural distribution of dopamine and serotonin. Our SBM analysis findings were consistent with reward-related neuroadaptations in the striato-thalamo-cortical and limbic pathways and also exhibited co-localization with the distribution of dopamine and serotonin systems. The moderation analysis suggested that the average dosage positively strengthens cocaine consumption years' effect on brain structures. By integrating our findings of gray and white matter volume differences and corresponding neurotransmitter profiles, this comprehensive view not only strengthens our understanding of the brain's structural abnormalities in CUD, but also reveals potential mechanisms underlying its development and progression.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142376322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comparing psilocybin to metformin as neuroprotective agents against Parkinson's dementia: A systematic review of evidence and efficacy. 比较迷幻药和二甲双胍作为帕金森痴呆症的神经保护剂：对证据和疗效的系统回顾。

IF 5.3 2区医学

Progress in Neuro-Psychopharmacology & Biological Psychiatry Pub Date : 2024-09-30 DOI: 10.1016/j.pnpbp.2024.111155

Randall D Ordovich-Clarkson, Maurice Jabbour, Daniel Arteaga Pelayo, Daniel Lara, Sebastian La Croix, Macie Mumman, Shoshanah Stukas, Reagan Anderson, David Meraz, Anthony Bangura, Brooklyn Anderson, Luke Bamrud, Caleb Blake

{"title":"Comparing psilocybin to metformin as neuroprotective agents against Parkinson's dementia: A systematic review of evidence and efficacy.","authors":"Randall D Ordovich-Clarkson, Maurice Jabbour, Daniel Arteaga Pelayo, Daniel Lara, Sebastian La Croix, Macie Mumman, Shoshanah Stukas, Reagan Anderson, David Meraz, Anthony Bangura, Brooklyn Anderson, Luke Bamrud, Caleb Blake","doi":"10.1016/j.pnpbp.2024.111155","DOIUrl":"10.1016/j.pnpbp.2024.111155","url":null,"abstract":"<p><strong>Background & aim: </strong>Treatment of Parkinson's disease (PD) has remained largely unchanged and focuses primarily on symptomatic relief through activation of dopaminergic pathways. Currently, there are no proven prophylactic approaches to the prevention of PD. This systematic review seeks to compare two separate compounds, metformin (MTF) and psilocybin, as potential prophylactic therapeutics against the development of PD.</p><p><strong>Methods: </strong>The authors conducted a systematic review focusing on primary studies that test these compounds on cell and animal models to determine if they might have any neuroprotective or neuroplastic effects.</p><p><strong>Results: </strong>The results of this review found that MTF may halt the progression of diseases such as PD through multiple mechanisms including reduced oxidative stress at the level of the mitochondria, thereby reducing α-synuclein related damage. Psilocybin, on the other hand, may increase repair of damaged neurons through psychoplastogenic activation of serotonergic pathways, particularly 5-HT<sub>2A</sub> receptor activation, ultimately increasing the release of brain derived neurotropic factor (BDNF) and the reduction of α-synuclein accumulation.</p><p><strong>Conclusion: </strong>Implications of this study include a need for further research in off-label use of MTF as well as further research into serotonergic compounds such as psilocybin for the treatment and prevention of neurodegenerative diseases.</p>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0