Molecular Neurobiology最新文献_第2页

Mechanisms of Senegenin in Regulating Oxidative Stress and Mitochondria Damage for Neuroprotection in Insomnia: Evidence from In Vivo and In Vitro Models. 人参皂苷元调节氧化应激和线粒体损伤对失眠症神经保护的机制：来自体内和体外模型的证据

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-04 DOI: 10.1007/s12035-025-05170-3

Honglin Jia, Zhengting Liang, Deqi Yan, Xu Chen, Ruining Liang, Jinhong Wu, Xingping Zhang

{"title":"Mechanisms of Senegenin in Regulating Oxidative Stress and Mitochondria Damage for Neuroprotection in Insomnia: Evidence from In Vivo and In Vitro Models.","authors":"Honglin Jia, Zhengting Liang, Deqi Yan, Xu Chen, Ruining Liang, Jinhong Wu, Xingping Zhang","doi":"10.1007/s12035-025-05170-3","DOIUrl":"https://doi.org/10.1007/s12035-025-05170-3","url":null,"abstract":"Insomnia is a common sleep disorder worldwide, and oxidative stress and mitochondrial damage are closely related to insomnia. This study aimed to investigate the mechanism by which senegenin exerts neuroprotective effects in regulating oxidative stress and mitochondrial damage in insomnia. In vivo, EEG/EMG analysis confirmed the successful establishment of insomnia rat models; Nissl and HE staining and electron microscopy were used to evaluate the pathological changes of neurons and mitochondria in rat brain tissue. The expression of oxidative stress and sleep factors was assessed. In vitro, an oxidative damage cell model was established to measure oxidative stress-related parameters; the protective concentration of senegenin against oxidative damage was determined using the CCK-8 assay, and the effects of senegenin on the expression of Keap1/Nrf2 and PINK1/Parkin, key signaling pathways involved in oxidative stress and mitochondrial damage, were analyzed. During insomnia, wake is prolonged, and NREM and REM are shortened; learning memory and exploration behavior are impaired, oxidative stress factor expression is changed, and mitochondria are damaged. Brain tissue from insomnia rats showed decreased BDNF, 5-HT1A, GABA-T, and GAD and increased expression of 5-HT2A and Glu. Keap1, PINK1, Parkin, and LC3 expression increased and Nrf2, NQO1, HO-1, and p62 expression decreased in oxidatively injured cells. Senegenin showed a dose-response regulatory effect after the intervention. Senegenin may exert neuroprotective effects in insomnia by improving oxidative stress and mitochondrial damage.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560529","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

PET Imaging Unveils Neuroinflammatory Mechanisms in Psychiatric Disorders: From Microglial Activation to Therapeutic Innovation. PET成像揭示精神疾病的神经炎症机制：从小胶质细胞激活到治疗创新。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-04 DOI: 10.1007/s12035-025-05177-w

Yu-Dan Liu, Yi-Heng Chang, Xue-Ting Xie, Xin-Yao Wang, Hao-Yan Ma, Mei-Chen Liu, Hui-Min Zhang

{"title":"PET Imaging Unveils Neuroinflammatory Mechanisms in Psychiatric Disorders: From Microglial Activation to Therapeutic Innovation.","authors":"Yu-Dan Liu, Yi-Heng Chang, Xue-Ting Xie, Xin-Yao Wang, Hao-Yan Ma, Mei-Chen Liu, Hui-Min Zhang","doi":"10.1007/s12035-025-05177-w","DOIUrl":"https://doi.org/10.1007/s12035-025-05177-w","url":null,"abstract":"Recent advancements in neuroinflammation research have significantly enhanced our understanding of its pivotal role in the pathogenesis and pathophysiology of psychiatric disorders. Positron emission tomography (PET) imaging, leveraging its unique ability to quantify biological processes in vivo non-invasively, has emerged as a transformative tool for investigating neuroimmune mechanisms. The 18 kDa translocator protein (TSPO), a biomarker of activated microglia and astrocytes during neuroinflammation, enables PET-based visualization of neuroinflammatory activity, offering novel insights into the neurobiological underpinnings of psychiatric conditions. This review synthesizes recent TSPO PET imaging findings across major psychiatric disorders, including major depressive disorder (MDD), obsessive-compulsive disorder (OCD), posttraumatic stress disorder (PTSD), schizophrenia, and psychosis. We critically evaluate how TSPO PET elucidates neuroinflammatory signatures linked to disease progression, treatment responses, and therapeutic stratification. Furthermore, we explore the translational potential of anti-inflammatory agents (e.g., celecoxib and minocycline) and TSPO-targeted ligands (e.g., etifoxine and XBD173) in modulating neurosteroid synthesis and neuroimmune interactions. By bridging methodological innovations with clinical applications, this review underscores the promise of TSPO PET in advancing diagnostic precision, personalized treatment strategies, and mechanistic insights into neuroinflammation-driven psychiatric pathologies. Challenges such as genetic polymorphisms (e.g., rs6971), partial volume effects (PVEs), and quantification biases are discussed to guide future research directions.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560530","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

Mbnl1 Protects Against Cerebral Ischemia-Reperfusion Injury by Modulating Microglia/Macrophage Polarization via NF-κB Pathway. Mbnl1通过NF-κB通路调节小胶质细胞/巨噬细胞极化，保护脑缺血再灌注损伤。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-03 DOI: 10.1007/s12035-025-05180-1

Wenting Xu, Mengjia Zhou, Linlin Li, Yuqing Zhang, Tianya Zhang, Xiangjian Zhang

{"title":"Mbnl1 Protects Against Cerebral Ischemia-Reperfusion Injury by Modulating Microglia/Macrophage Polarization via NF-κB Pathway.","authors":"Wenting Xu, Mengjia Zhou, Linlin Li, Yuqing Zhang, Tianya Zhang, Xiangjian Zhang","doi":"10.1007/s12035-025-05180-1","DOIUrl":"https://doi.org/10.1007/s12035-025-05180-1","url":null,"abstract":"Activated and polarized microglia regulate neuroinflammatory responses and programmed cell death processes in ischemic stroke. Although the inactivation of muscleblind-like 1 (Mbnl1) is known to cause structural defects in the brain, its role in microglial apoptosis and polarization remains unclear. This study aims to explore the mechanism of Mbnl1 in ischemic stroke, particularly its role in the regulation of microglial apoptosis and polarization, as well as its impact on neuroinflammatory responses and cognitive dysfunction. The expression level of Mbnl1 in the serum of stroke patients was determined. Furthermore, Mbnl1 was overexpressed in a C57BL/6N stroke model and an oxygen-glucose deprivation model in BV-2 cells. Changes in relevant marker proteins were detected using histological assays, cognitive function tests, enzyme-linked immunosorbent assay for inflammatory factor detection, flow cytometry for apoptosis assessment, immunofluorescence, and Western blot analysis. The expression level of Mbnl1 in the serum of stroke patients was determined. Furthermore, Mbnl1 was overexpressed in a C57BL/6N stroke model and an oxygen-glucose deprivation model in BV-2 cells. Changes in relevant marker proteins were detected using histological assays, cognitive function tests, enzyme-linked immunosorbent assay for inflammatory factor detection, flow cytometry for apoptosis assessment, immunofluorescence, and Western blot analysis. Mbnl1 overexpression exerts a protective effect against ischemic stroke by regulating microglia-mediated neuroinflammation through inhibition of the NF-κB signaling pathway. This modulation promotes cognitive recovery in C57BL/6N mice with stroke, highlighting Mbnl1 as a potential therapeutic target for stroke treatment.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553990","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

G-Protein-Coupled Receptor-Microtubule Interactions Regulate Neurite Development and Protect Against β-Amyloid Neurotoxicity. g蛋白偶联受体-微管相互作用调节神经突发育并防止β-淀粉样蛋白神经毒性。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-02 DOI: 10.1007/s12035-025-05179-8

Sneha Singh, Ujendra Kumar

{"title":"G-Protein-Coupled Receptor-Microtubule Interactions Regulate Neurite Development and Protect Against β-Amyloid Neurotoxicity.","authors":"Sneha Singh, Ujendra Kumar","doi":"10.1007/s12035-025-05179-8","DOIUrl":"https://doi.org/10.1007/s12035-025-05179-8","url":null,"abstract":"G-protein-coupled receptors (GPCRs) regulate multiple cellular functions, including neurite formation and maturation, processes often disrupted in neurodegenerative diseases. Like GPCRs, microtubule-associated proteins (MAPs, including MAP2 and Tuj1) and the synaptic vesicle protein synaptophysin are essential for neurite formation, maturation, and organization, which underpin brain development and cognitive function. Despite their importance, the functional crosstalk between GPCRs and MAPs, particularly in neurogenesis and pathological conditions such as Alzheimer's disease (AD), remains poorly understood. We show that somatostatin and dopamine receptors (SSTR and DR) are the structural anchors in developing neurites, enabling MAP recruitment and synaptic protein localization. Our findings reveal a cAMP-dependent interplay involving PTEN and ERK1/2, modulating neurite formation and MAPs organization. Notably, we show that β-amyloid (Aβ) disrupts the constitutive association of MAP2 and Tuj1, inducing an increase in intracellular cAMP levels, loss of neurite integrity, and impaired neuronal viability. The activation of SSTR and DR signaling restores neurite architecture and synaptic integrity via p-AKT activation and PTEN inhibition, highlighting a neuroprotective mechanism. Together, our results reveal a novel role of GPCRs in orchestrating interactions with MAPs to regulate neuronal maturation, neurite formation, and synaptic integrity. This study provides a new mechanistic rationale for therapeutic strategies aimed at preserving cognitive function in neurological disorders such as AD.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540959","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

Pathway Analysis and Genetic Markers in Parkinson's Disease: Insights into Subtype-Specific Mechanisms. 帕金森病的通路分析和遗传标记：对亚型特异性机制的见解。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-02 DOI: 10.1007/s12035-025-05182-z

Sara Taremi Horoufi, Davood Zaeifi

{"title":"Pathway Analysis and Genetic Markers in Parkinson's Disease: Insights into Subtype-Specific Mechanisms.","authors":"Sara Taremi Horoufi, Davood Zaeifi","doi":"10.1007/s12035-025-05182-z","DOIUrl":"https://doi.org/10.1007/s12035-025-05182-z","url":null,"abstract":"Parkinson's disease (PD) is a complex disease influenced by both genetic and environmental factors. Despite advances in understanding PD genetics, subtype-specific mechanisms remain poorly characterized. This study aims to identify distinct genetic markers and pathways across PD subtypes, addressing this gap to enable targeted diagnostics and therapies. Genes associated with PD were collected from various databases and categorized into groups based on the PD type to assess the PD risk. Protein interaction analysis was conducted to identify functional clusters and key genes within each group. KEGG enrichment analysis revealed common genes and pathways among the different PD groups. This study conformed to the PRISMA 2020 guidelines for systematic data collection and analysis. Hub genes such as PRKN, SNCA, and LRRK2 have demonstrated considerable potential as biomarkers for genetic predisposition in PD, alongside the identification of additional complementary genes. Analysis of hub node variants highlighted specific genetic variations in these genes. We identified several microRNAs, including hsa-miR-335-5p, hsa-miR-19a-3p, and hsa-miR-106a-5p, as well as transcription factors that interact with crucial hub genes. This study refines subtype-specific mechanisms for established PD genes and identifies novel genetic markers and pathways associated with juvenile, young-onset, late-onset, familial, and sporadic Parkinson's disease, enhancing our understanding of their molecular mechanisms and potential for targeted diagnostics and therapies. Specifically, we highlight the roles of hub genes, such as PRKN, SNCA, and LRRK2, alongside significant microRNA interactions, which may serve as biomarkers for early detection and personalized treatment approaches.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540960","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

The Efficacy of Intrathecal Platelet-Rich Plasma Administration in Alleviation of Chronic Neuropathic Pain in Rat Model. 鞘内富血小板血浆给药对大鼠慢性神经性疼痛的缓解作用。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-02 DOI: 10.1007/s12035-025-05173-0

Jaisan Islam, Preeti Kumari Chaudhary, Sanggu Kim, Elina Kc, Young Seok Park, Soochong Kim

{"title":"The Efficacy of Intrathecal Platelet-Rich Plasma Administration in Alleviation of Chronic Neuropathic Pain in Rat Model.","authors":"Jaisan Islam, Preeti Kumari Chaudhary, Sanggu Kim, Elina Kc, Young Seok Park, Soochong Kim","doi":"10.1007/s12035-025-05173-0","DOIUrl":"https://doi.org/10.1007/s12035-025-05173-0","url":null,"abstract":"Chronic neuropathic pain (CNP), marked by various stinging sensations, frequently arises from lumbosacral disorders, where astrocytes in the spinal dorsal horn (SDH) significantly contribute to its persistence. Platelet-rich plasma (PRP) treatment has shown regulatory effects on astrocytic activity in inflammatory and diabetic neuropathy, yet its impact on CNP remains unclear. This study investigates the potential of intrathecal PRP injections for mitigating CNP in a chronic compressed dorsal root ganglion (CCD) rat model. Animals were divided into CCD, sham, and control groups. PRP or phosphate-buffered saline (PBS) was injected intrathecally between the L4-L5 spinal cord. Assessments included mechanical and thermal pain behavioral tests, and in vivo extracellular recordings from the contralateral ventral posterolateral (VPL) thalamus. Additionally, the expression of astrocytic pain mediators in the SDH was analyzed through immunofluorescence. Results showed that the CCD group had significantly lower pain thresholds compared to the sham group. PRP treatment led to improved CNP responses in CCD rats, unlike in the PBS group, highlighting PRP's role in CNP amelioration. Electrophysiology confirmed a notable reduction in VPL thalamic activity post-PRP treatment. Immunofluorescence (IFC) analysis revealed significant increases in neuronal c-fos expression in the DRG and SDH of CCD rats, which were notably reduced following PRP treatment. IFC analysis also indicated decreased expression of pain-transmission-associated astrocyte markers, including glial fibrillary acidic protein (GFAP), pyruvate kinase M2 (PKM2), and high mobility group box-1 protein (HMGB1) in PRP-treated CCD subjects. Thus, we demonstrate that PRP attenuates CNP in a CCD rat model by regulating nociceptive input into the spinothalamic tract through the inhibition of astrocytic activity in SDH, presenting itself as a viable therapy for CNP linked to lumbosacral conditions.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540962","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

GPR139, an Ancient Receptor and an Emerging Target for Neuropsychiatric and Behavioral Disorders. GPR139，一种古老的受体和神经精神和行为障碍的新靶点。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-01 Epub Date: 2025-03-18 DOI: 10.1007/s12035-025-04828-2

Minyu Chan, Satoshi Ogawa

{"title":"GPR139, an Ancient Receptor and an Emerging Target for Neuropsychiatric and Behavioral Disorders.","authors":"Minyu Chan, Satoshi Ogawa","doi":"10.1007/s12035-025-04828-2","DOIUrl":"10.1007/s12035-025-04828-2","url":null,"abstract":"GPR139 is an orphan G-protein-coupled receptor that is predominantly expressed in several midbrain regions, e.g., the habenula, striatum, and hypothalamus. GPR139 gene is highly conserved across vertebrate phylogenetic taxa, suggesting its fundamental importance in neurophysiology. Evidence from both animal studies and human genetic association studies has demonstrated that dysregulation of GPR139 expression and function is linked to aberrant behaviors, cognitive deficits, alterations in sleep and alertness, and substance abuse and withdrawal. Animal knockout models suggest that GPR139 plays an anti-opioid role by modulating the signaling activity of the μ-opioid receptor (MOR), as well as the intensity of withdrawal symptoms and nociception in behavioral paradigms. Modulation of GPR139 activity by surrogate agonists such as TAK-041 and JNJ-63533054 has shown promising results in experimental models; however, the use of TAK-041 in clinical trials has produced heterogeneous effects and has not met the intended primary endpoint. Here, we highlight current in vitro and in vivo studies of GPR139, its potential physiological roles, and therapeutic potential in the pathophysiology of neuropsychiatric and behavioral disorders. This review aims to focus on the current knowledge gaps to facilitate future studies that will contribute to the understanding of GPR139 as a therapeutic target for neuropsychiatric and behavioral disorders.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"9324-9337"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657816","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

Decoding the Role of Neurotrophins in Glycogen Synthase Kinase 3-Beta Regulation in Alzheimer's Disease. 解码阿尔茨海默病中糖原合成酶激酶3- β调节中神经营养因子的作用。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-01 Epub Date: 2025-02-27 DOI: 10.1007/s12035-025-04776-x

Shubham Nilkanth Rahmatkar, Damanpreet Singh

{"title":"Decoding the Role of Neurotrophins in Glycogen Synthase Kinase 3-Beta Regulation in Alzheimer's Disease.","authors":"Shubham Nilkanth Rahmatkar, Damanpreet Singh","doi":"10.1007/s12035-025-04776-x","DOIUrl":"10.1007/s12035-025-04776-x","url":null,"abstract":"Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most prevalent contributor to dementia in elderly individuals. Numerous signalling pathways influencing AD pathophysiology, involving glycogen synthase kinase-3β (Gsk-3β), have been investigated extensively as potential therapeutic targets. Gsk-3β is a critical factor in AD pathogenesis that affects several key hallmarks of the disease notably tau phosphorylation, amyloid-β generation, cognition, neurogenesis, and synaptic integrity. Neurotrophins are small proteins that are critical for maintaining neuronal health and function and may be used to treat neurodegenerative diseases. Notably, the dysregulation of certain neurotrophins and their receptors is also linked with AD which is a major contributor to neurodegeneration. Studies indicated that neurotrophins and their modulators are capable of protecting neurons by blocking the Gsk-3β activity suggesting a potential link for neuroprotection. Neurotrophins support the survival of neurons by regulating Gsk-3β activity. Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) signalling pathways activate Trk receptors that trigger downstream signalling cascades that subsequently inhibit Gsk-3β activity and reduce AD-related neuropathology. We also explore the role of modulators including phosphatases, kinase cascades, and other regulatory proteins that cross paths with neurotrophin-Gsk-3β signalling. In conclusion, this manuscript summarizes both direct and indirect regulatory roles of neurotrophins and modulators on Gsk-3β to understand the intricate mechanisms driving neurodegeneration in AD.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8603-8623"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143516192","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

Nutritional Interventions in Amyotrophic Lateral Sclerosis: From Ketogenic Diet and Neuroprotective Nutrients to the Microbiota-Gut-Brain Axis Regulation. 肌萎缩性侧索硬化的营养干预：从生酮饮食和神经保护营养素到微生物-肠-脑轴调节。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-01 Epub Date: 2025-03-17 DOI: 10.1007/s12035-025-04830-8

Samira Nabakhteh, Anahita Lotfi, Arman Afsartaha, Elaheh Sadat Khodadadi, Siavash Abdolghaderi, Mozhdeh Mohammadpour, Yasaman Shokri, Pouria Kiani, Sajad Ehtiati, Sara Khakshournia, Seyyed Hossein Khatami

{"title":"Nutritional Interventions in Amyotrophic Lateral Sclerosis: From Ketogenic Diet and Neuroprotective Nutrients to the Microbiota-Gut-Brain Axis Regulation.","authors":"Samira Nabakhteh, Anahita Lotfi, Arman Afsartaha, Elaheh Sadat Khodadadi, Siavash Abdolghaderi, Mozhdeh Mohammadpour, Yasaman Shokri, Pouria Kiani, Sajad Ehtiati, Sara Khakshournia, Seyyed Hossein Khatami","doi":"10.1007/s12035-025-04830-8","DOIUrl":"10.1007/s12035-025-04830-8","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disease with significant challenges in diagnosis and treatment. Recent research has highlighted the complex nature of ALS, encompassing behavioral impairments in addition to its neurological manifestations. While several medications have been approved to slow disease progression, ongoing research is focused on identifying new therapeutic targets. The current review focuses on emerging therapeutic strategies and personalized approaches aimed at improving patient outcomes. Recent advancements highlight the importance of targeting additional pathways such as mitochondrial dysfunction and neuroinflammation to develop more effective treatments. Personalized medicine, including genetic testing and biomarkers, is proving valuable in stratifying patients and tailoring treatment options. Complementary therapies, such as nutritional interventions like the ketogenic diet and microbiome modulation, also show promise. This review emphasizes the need for a multidisciplinary approach that integrates early diagnosis, targeted treatments, and supportive care to address the multisystemic nature of ALS and improve the quality of life for patients.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"9216-9239"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649624","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

Sustaining Brain Youth by Neural Stem Cells: Physiological and Therapeutic Perspectives. 神经干细胞维持大脑青春：生理和治疗观点。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2025-07-01 Epub Date: 2025-02-22 DOI: 10.1007/s12035-025-04774-z

Matilde Santos, João A Ferreira Moreira, Sónia Sá Santos, Susana Solá

{"title":"Sustaining Brain Youth by Neural Stem Cells: Physiological and Therapeutic Perspectives.","authors":"Matilde Santos, João A Ferreira Moreira, Sónia Sá Santos, Susana Solá","doi":"10.1007/s12035-025-04774-z","DOIUrl":"10.1007/s12035-025-04774-z","url":null,"abstract":"In the last two decades, stem cells (SCs) have attracted considerable interest for their research value and therapeutic potential in many fields, namely in neuroscience. On the other hand, the discovery of adult neurogenesis, the process by which new neurons are generated in the adult brain, challenged the traditional view that the brain is a static structure after development. The recent findings showing that adult neurogenesis has a significant role in brain plasticity, learning and memory, and emotional behavior, together with the fact that it is strongly dependent on several external and internal factors, have sparked more interest in this area. The mechanisms of adult neural stem cell (NSC) regulation, the physiological role of NSC-mediated neuroplasticity throughout life, and the most recent NSC-based therapeutic applications will be concisely reviewed. Noteworthy, due to their multipotency, self-renewal potential, and ability to secrete growth and immunomodulatory factors, NSCs have been mainly suggested for (1) transplantation, (2) neurotoxicology tests, and (3) drug screening approaches. The clinical trials of NSC-based therapy for different neurologic conditions are, nonetheless, mostly in the early phases and have not yet demonstrated conclusive efficacy or safety. Here, we provide an outlook of the major challenges and limitations, as well as some promising directions that could help to move toward stem cell widespread use in the treatment and prevention of several neurological disorders.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8222-8247"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476757","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