Valerio Ricci, Domenico De Berardis, Giovanni Martinotti, Giuseppe Maina
{"title":"Glial Derived Neurotrophic Factor and Schizophrenia Spectrum Disorders: A Scoping Review.","authors":"Valerio Ricci, Domenico De Berardis, Giovanni Martinotti, Giuseppe Maina","doi":"10.2174/011570159X340124241205095729","DOIUrl":"https://doi.org/10.2174/011570159X340124241205095729","url":null,"abstract":"<p><strong>Background: </strong>Psychotic disorders, characterized by altered brain function, significantly impair reality perception. The neurodevelopmental hypothesis suggests these disorders originate from early brain development disruptions. Glial-derived neurotrophic factor (GDNF) is crucial for neuronal survival and differentiation, especially in dopaminergic neurons, and shows promise in neurodegenerative and neuropsychiatric conditions.</p><p><strong>Objectives: </strong>This scoping review aims to examine the role of GDNF in schizophrenia spectrum disorders and substance-induced psychoses, integrating knowledge on the neurobiological mechanisms and therapeutic potential of GDNF.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted using PubMed and Scopus databases from January 2001 onwards. Data extraction focused on GDNF levels, cognitive function, antipsychotic treatment effects, and genetic studies.</p><p><strong>Results: </strong>The review included 25 studies (18 human, 7 animal). While some studies demonstrated inconsistent results regarding GDNF serum levels in schizophrenic patients, the majority reported correlations between GDNF levels and cognitive functions. Animal studies underscored GDNF's role in stress response, drug-induced neurotoxicity, and dopamine signaling abnormalities. Genetic studies revealed potential associations between GDNF gene polymorphisms and schizophrenia susceptibility, though findings were mixed.</p><p><strong>Discussion: </strong>GDNF plays a significant role in cognitive functions and neuroprotection in schizophrenia. The variability in study results underscores the complexity of GDNF's involvement. The therapeutic potential of GDNF in psychotic disorders remains unclear, necessitating further research to clarify its efficacy and safety.</p><p><strong>Conclusion: </strong>This review emphasizes the importance of integrated biomarker strategies, gene therapy approaches, and precision medicine in advancing the understanding and treatment of psychotic disorders.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827739","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}
{"title":"Efficacy and Safety of Natural Apigenin Treatment for Alzheimer's Disease: Focus on In vivo Research Advancements.","authors":"Nan Zhang, Jianfei Nao, Xiaoyu Dong","doi":"10.2174/1570159X23666241211095018","DOIUrl":"https://doi.org/10.2174/1570159X23666241211095018","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's Disease (AD) is the most common dementia in clinics. Despite decades of progress in the study of the pathogenesis of AD, clinical treatment strategies for AD remain lacking. Apigenin, a natural flavonoid compound, is present in a variety of food and Chinese herbs and has been proposed to have a wide range of therapeutic effects on dementia.</p><p><strong>Objective: </strong>To clarify the relevant pharmacological mechanism and therapeutic effect of apigenin on animal models of AD.</p><p><strong>Methods: </strong>Computer-based searches of the PubMed, Cochrane Library, Embase, and Web of Science databases were used to identify preclinical literature on the use of apigenin for treating AD. All databases were searched from their respective inception dates until June 2023. The meta-analysis was performed with Review manager 5.4.1 and STATA 17.0.</p><p><strong>Results: </strong>Thirteen studies were eventually enrolled, which included 736 animals in total. Meta-analysis showed that apigenin had a positive effect on AD. Compared to controls, apigenin treatment reduced escape latency, increased the percentage of time spent in the target quadrant and the number of plateaus traversed; apigenin was effective in reducing nuclear factor kappa-B (NF-κB) p65 levels; apigenin effectively increased antioxidant molecules SOD and GSH-px and decreased oxidative index MDA; for ERK/CREB/BDNF pathway, apigenin effectively increased BDNF and pCREB molecules; additionally, apigenin effectively decreased caspase3 levels and the number of apoptotic cells in the hippocampus.</p><p><strong>Conclusion: </strong>The results show some efficacy of apigenin in the treatment of AD models. However, further clinical studies are needed to confirm the clinical efficacy of apigenin.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812663","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}
Antonietta Arcella, Marika Alborghetti, Anna Traficante, Maria Antonietta Oliva, Sabrina Staffieri, Veronica Russo, Matteo Caridi, Giuseppe Battaglia
{"title":"Pharmacological Blockade of Group II Metabotropic Glutamate Receptors Reduces the Incidence of Brain Tumors Induced by Prenatal Exposure to N-ethyl-N-nitrosourea in Rats.","authors":"Antonietta Arcella, Marika Alborghetti, Anna Traficante, Maria Antonietta Oliva, Sabrina Staffieri, Veronica Russo, Matteo Caridi, Giuseppe Battaglia","doi":"10.2174/1570159X23666241209090326","DOIUrl":"https://doi.org/10.2174/1570159X23666241209090326","url":null,"abstract":"<p><strong>Background: </strong>The study demonstrates that pharmacological blockade of type 3 metabotropic glutamate (mGlu3) receptors at the time of tumor induction significantly reduces the incidence of brain gliomas in rats. The overall survival of patients with high-grade brain gliomas is 14-20 months after current multimodal therapy, including surgery, radiotherapy, and adjuvant chemotherapy.</p><p><strong>Objective: </strong>To demonstrate in this experimental model that pharmacological blockade of group II metabotropic glutamate receptors reduces the incidence of brain tumors induced by prenatal exposure to N- ethyl-N-nitrosourea (ENU) in rats.</p><p><strong>Methods: </strong>Dams received a single injection of ENU (40 mg/kg, e.v.) at day 20 of pregnancy, combined with 5 daily injections of either saline or the mGlu2/3 receptor antagonist, LY341495 (10 mg/kg) (from day 15 to day 21 of pregnancy). Assessment of brain tumors in the offspring at 5 months of age showed the presence of mixed gliomas (astrocytomas/oligodendrogliomas) in 70% of the ENU + saline group of rats and only in 30% of the ENU + LY341495 group.</p><p><strong>Conclusion: </strong>Tumors in both groups of rats showed a moderate/high expression of the astrocyte marker, GFAP, and the oligodendrocyte marker, OLIG-2, and a low expression of the proliferation marker, Ki-67. However, tumors of the ENU + LY341495 group showed a reduced density of Iba-1+ cells, suggesting a lower extent of neuroinflammation in the tumor microenvironment. These findings strengthen the hypothesis that mGlu3 receptors are candidate drug targets for the treatment of malignant gliomas.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817507","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}
Runyi Mao, Sufang Liu, John C Dolan, Brian L Schmidt, Feng Tao
{"title":"Programmed Cell Death Protein 1 Contributes to Oral Cancer Pain via Regulating Tumor Necrosis Factor Alpha in the Spinal Trigeminal Nucleus Caudalis.","authors":"Runyi Mao, Sufang Liu, John C Dolan, Brian L Schmidt, Feng Tao","doi":"10.2174/1570159X23666241209160039","DOIUrl":"https://doi.org/10.2174/1570159X23666241209160039","url":null,"abstract":"<p><strong>Background: </strong>Oral cancer causes intense pain at the primary site, and such pain can impair oral functions. However, the underlying mechanisms for oral cancer pain are still not fully understood. In the present study, it is investigated whether programmed cell death protein 1 (PD-1) is involved in the development of oral cancer pain.</p><p><strong>Methods: </strong>RMP1-14, a specific anti-PD-1 antibody, was injected into spinal trigeminal nucleus caudalis (Sp5C) and measured pain behaviors using von Frey filaments and dolognawmeter. Western blotting and immunofluorescence staining were performed to analyze the expression of PD-1 and tumor necrosis factor alpha (TNFα) in the Sp5C.</p><p><strong>Results: </strong>It was observed that the PD-1 antibody significantly inhibited mechanical hypersensitivity and functional allodynia in our oral cancer pain mouse model. Moreover, we found that TNFα was highly upregulated in the Sp5C following the induction of oral cancer pain and that intra-Sp5C injection of the PD-1 antibody diminished the upregulation of TNFα. It was found that genetic deletion of TNFα or its receptor antagonism synergized the analgesic effect of PD-1 antibody on oral cancer pain.</p><p><strong>Conclusion: </strong>Our results suggest that PD-1 in the Sp5C contributes to oral cancer pain by altering TNFα signaling in the trigeminal nociceptive system, and PD-1 could be targeted to develop a novel approach for oral cancer pain management.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806438","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}
Marialuisa de Ceglia, Adele Romano, Maria Vittoria Micioni Di Bonaventura, Ana Gavito, Luca Botticelli, Emanuela Micioni Di Bonaventura, Marzia Friuli, Carlo Cifani, Fernando Rodríguez de Fonseca, Silvana Gaetani
{"title":"Cafeteria Diet Abstinence Induces Depressive Behavior and Disrupts Endocannabinoid Signaling in Dopaminergic Areas: A Preclinical Study.","authors":"Marialuisa de Ceglia, Adele Romano, Maria Vittoria Micioni Di Bonaventura, Ana Gavito, Luca Botticelli, Emanuela Micioni Di Bonaventura, Marzia Friuli, Carlo Cifani, Fernando Rodríguez de Fonseca, Silvana Gaetani","doi":"10.2174/1570159X23666241107160840","DOIUrl":"10.2174/1570159X23666241107160840","url":null,"abstract":"<p><strong>Background: </strong>Alterations of dopamine (DA) transmission in the brain reward system can be associated with an addictive-like state defined as food addiction (FA), common in obese individuals. Subjects affected by FA experience negative feelings when abstinent from their preferred diet and may develop mood disorders, including depression, sustained by alterations in brain DA pathways.</p><p><strong>Objective: </strong>This study aims to investigate the impact of long-term abstinence from a palatable diet on depressive-like behavior in rats, exploring neurochemical alterations in monoamine and endocannabinoid signaling in DA-enriched brain regions, including ventral tegmental area, dorsolateral striatum, substantia nigra and medial prefrontal cortex.</p><p><strong>Methods: </strong>Rats underwent exposure and subsequent abstinence from a palatable cafeteria diet. During abstinence, animals were treated with fatty acid amide hydrolase (FAAH) inhibitor PF-3845 (10 mg/kg, intraperitoneal administration every other day). Lastly, animals were subjected to a forced swimming test, and their brains were dissected and processed for high-performance liquid chromatography measurement of monoamines and western blot analyses of markers of the endocannabinoid machinery.</p><p><strong>Results: </strong>After the withdrawal from the palatable diet, animals showed depressive-like behavior, coupled with significant variations in the concentration of brain monoamines and in the expression of endocannabinoid signalling machinery proteins in cited brain areas. Treatment with PF-3845 exerted an antidepressant- like effect and restored part of the alterations in monoaminergic and endocannabinoid systems.</p><p><strong>Conclusion: </strong>Overall, our results suggest that abstinence from a cafeteria diet provokes emotional disturbances linked to neuroadaptive changes in monoamines and endocannabinoid signalling in brain areas partaking to DA transmission that could partially be restored by the enhancement of endocannabinoid signalling through FAAH inhibition.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709428","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}
Liza Changkakoti, Rajan Rajabalaya, Sheba R David, Ashok Kumar Balaraman, Hemalatha Sivasubramanian, Ashis K Mukherjee, Asis Bala
{"title":"Exploration of the Role of Vitamins in Preventing Neurodegenerative Diseases: Comprehensive Review on Preclinical and Clinical Findings.","authors":"Liza Changkakoti, Rajan Rajabalaya, Sheba R David, Ashok Kumar Balaraman, Hemalatha Sivasubramanian, Ashis K Mukherjee, Asis Bala","doi":"10.2174/011570159X327677240902105443","DOIUrl":"https://doi.org/10.2174/011570159X327677240902105443","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) are a multifaceted and heterogeneous group of complex diseases. Unfortunately, a cure for these conditions has yet to be found, but there are ways to reduce the risk of developing them. Studies have shown that specific vitamins regulate the brain molecules and signaling pathways, which may help prevent degeneration. This review focuses on examining the role of vitamins in preventing five significant types of neurodegenerative diseases, including Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). This review also highlights promising and controversial findings about the potential impact of vitamins on this group of diseases. Several developed countries standardize daily dietary vitamin intake to meet nutrient requirements, improve health, and prevent chronic diseases like NDDs. However, more research is necessary to gain a more comprehensive understanding of their therapeutic benefits, including studies exploring different drug-dose paradigms, diverse humanized animal models, and clinical trials conducted in various locations.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686043","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}
Maria Di Chiara, Gianluca Terrin, Marco Fiore, Maria Chiara De Nardo, Gianluigi Laccetta, Flavia Gloria, Antonio Minni, Christian Barbato, Carla Petrella
{"title":"Early Enteral Feeding Restores Neurofilament Light Chain Serum Levels in Preterm Newborns.","authors":"Maria Di Chiara, Gianluca Terrin, Marco Fiore, Maria Chiara De Nardo, Gianluigi Laccetta, Flavia Gloria, Antonio Minni, Christian Barbato, Carla Petrella","doi":"10.2174/1570159X23666240920165612","DOIUrl":"https://doi.org/10.2174/1570159X23666240920165612","url":null,"abstract":"<p><strong>Background: </strong>Positive effects of early nutritional strategies on neurological outcomes have been observed when nutrients were administered by the enteral route, especially during the first week of life. Evidence reports that serum neurofilament light chain (NfL), a structural protein of neurons, is a specific and reliable biomarker of neuronal damage.</p><p><strong>Objective: </strong>The present study aimed to investigate the effect of early enteral nutrition (EN) in minimizing neuroaxonal damage and assessing NfL serum levels in preterm neonates.</p><p><strong>Methods: </strong>Fifty-four preterm neonates without severe brain impairment and 20 full-term babies as controls were enrolled from the Neonatal Intensive Care Unit at the Policlinico Umberto I in Rome. We performed blood sampling at birth (day of life 0 - DoL 0) in 20 full-term newborns and in 19 pre-term infants. Furthermore, we executed blood sampling at DoL 28 in other 22 pre-term newborns who received early enteral nutrition (EN) within the third DoL (Early-EN) and in 13 other pre-term newborns who received EN after the third DoL (Late-EN).</p><p><strong>Results: </strong>Serum levels of NfL were higher in preterm babies when compared to full-term neonates, at DoL 0 (48.81 ± 9.4 vs. 11.67 ± 1.4 pg/ml; p = 0.007). Interestingly, at DoL 28, serum NfL was significantly decreased in the Early-EN newborns compared to the Late-EN groups (15.22 ± 2.0 vs. 50.05 ± 17.9 pg/ml; p = 0.03).</p><p><strong>Conclusions: </strong>It was shown that early enteral feeding, within the first week of life, could be a useful tool for limiting neurological impairment in pre-term neonates by restoring NfL.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603600","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}
Adrián S Elliott, Román D Moreno-Fernández, Patricia Sampedro-Piquero
{"title":"Effects of Alcohol on EEG Activity: A Systematic Review Focused on Sex-Related Differences in Youth.","authors":"Adrián S Elliott, Román D Moreno-Fernández, Patricia Sampedro-Piquero","doi":"10.2174/1570159X23666241106095027","DOIUrl":"10.2174/1570159X23666241106095027","url":null,"abstract":"<p><strong>Background: </strong>Most electroencephalographic (EEG) investigations on alcohol have focused on adults, and scarce data is available about the potential of EEG measurements to detect young people at high-risk, as well as, to understand possible sex differences in alcohol impact on the brain.</p><p><strong>Objective: </strong>This systematic review aimed to explore sex-related differences in EEG among young people with alcohol misuse, alcohol use disorder (AUD), and offspring of families with AUD.</p><p><strong>Methods: </strong>A systematic review of the literature was conducted following PRISMA guidelines. Review protocol was registered in Prospero (ID: CRD42024511471). After article selection process and quality assessment, 25 studies were included in our review. The search included participants between 12 and 30 years old with problematic alcohol consumption, as defined by DSM, AUDIT, or specific alcohol misuse questionnaires.</p><p><strong>Results: </strong>It seems that beta was generally higher in young males with AUD, and they usually exhibited greater interhemispheric connectivity (interHC), whereas young females with AUD tended towards enhanced intraHC. P3 appears to be particularly sensitive to alcohol misuse, with males typically exhibiting a lower amplitude than young females. Other event related potentials (ERPs) such as N415, P640, and the error-related negativity (ERN) lacked sufficient methodological support to draw conclusions regarding sex differences, N340 and P540 suggested avenues for expanding research on memory processing, indicating differences in amplitude between males and females.</p><p><strong>Conclusion: </strong>Considering sex variables in clinical research will enhance our understanding of alterations in brain function and structure with the goal of tailoring treatment strategies for AUD.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590456","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}
{"title":"Neuropsychiatric Manifestations of COVID-19 Disease and Post Covid Syndrome: The Role of N Acetyl-cysteine and Acetyl-L-carnitine.","authors":"Tommaso Barlattani, Giuseppe Celenza, Alessandro Cavatassi, Franco Minutillo, Valentina Socci, Carolina Pinci, Riccardo Santini, Francesca Pacitti","doi":"10.2174/011570159X343115241030094848","DOIUrl":"10.2174/011570159X343115241030094848","url":null,"abstract":"<p><p>COVID-19 is associated with neuropsychiatric symptoms, such as anosmia, anxiety, depression, stress-related reactions, and psychoses. The illness can cause persistent cognitive impairment and \"brain fog\", suggesting chronic brain involvement. Clinical entities of ongoing symptomatic COVID-19 and Post COVID Syndrome (PCS) mainly present neuropsychiatric symptoms such as dysgeusia, headache, fatigue, anxiety, depression, sleep disturbances, and post-traumatic stress disorder. The pathophysiology of COVID-19-related brain damage is unclear, but it is linked to various mechanisms such as inflammation, oxidative stress, immune dysregulation, impaired glutamate homeostasis, glial and glymphatic damage, and hippocampal degeneration. Noteworthy is that the metabotropic receptor mGluR2 was discovered as a mechanism of internalisation of SARS-CoV-2 in Central Nervous System (CNS) cells. N-acetylcysteine (NAC) and acetyl-L-carnitine (ALC) are two supplements that have already been found effective in treating psychiatric conditions. Furthermore, NAC showed evidence in relieving cognitive symptomatology in PCS, and ALC was found effective in treating depressive symptomatology of PCS. The overlapping effects on the glutamatergic system of ALC and NAC could help treat COVID-19 psychiatric symptoms and PCS, acting through different mechanisms on the xc-mGluR2 network, with potentially synergistic effects on chronic pain and neuro-astrocyte protection. This paper aims to summarise the current evidence on the potential therapeutic role of NAC and ALC, providing an overview of the underlying molecular mechanisms and pathophysiology. It proposes a pathophysiological model explaining the effectiveness of NAC and ALC in treating COVID-19-related neuropsychiatric symptoms.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589314","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}
Tong Nie, Li You, Fang Tang, Yanhui Duan, Eugenie Nepovimova, Kamil Kuca, Qinghua Wu, Wei Wei
{"title":"Microbiota-Gut-Brain Axis in Age-Related Neurodegenerative Diseases.","authors":"Tong Nie, Li You, Fang Tang, Yanhui Duan, Eugenie Nepovimova, Kamil Kuca, Qinghua Wu, Wei Wei","doi":"10.2174/1570159X23666241101093436","DOIUrl":"https://doi.org/10.2174/1570159X23666241101093436","url":null,"abstract":"<p><strong>Background: </strong>Age-related neurodegenerative diseases (NDs) pose a formidable challenge to healthcare systems worldwide due to their complex pathogenesis, significant morbidity, and mortality. Scope and Approach: This comprehensive review aims to elucidate the central role of the microbiotagut- brain axis (MGBA) in ND pathogenesis. Specifically, it delves into the perturbations within the gut microbiota and its metabolomic landscape, as well as the structural and functional transformations of the gastrointestinal and blood-brain barrier interfaces in ND patients. Additionally, it provides a comprehensive overview of the recent advancements in medicinal and dietary interventions tailored to modulate the MGBA for ND therapy.</p><p><strong>Conclusion: </strong>Accumulating evidence underscores the pivotal role of the gut microbiota in ND pathogenesis through the MGBA. Dysbiosis of the gut microbiota and associated metabolites instigate structural modifications and augmented permeability of both the gastrointestinal barrier and the blood-brain barrier (BBB). These alterations facilitate the transit of microbial molecules from the gut to the brain via neural, endocrine, and immune pathways, potentially contributing to the etiology of NDs. Numerous investigational strategies, encompassing prebiotic and probiotic interventions, pharmaceutical trials, and dietary adaptations, are actively explored to harness the microbiota for ND treatment. This work endeavors to enhance our comprehension of the intricate mechanisms underpinning ND pathogenesis, offering valuable insights for the development of innovative therapeutic modalities targeting these debilitating disorders.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582390","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}