Translational Neuroscience最新文献

{"title":"A comparative study of the impact of maternal immune activation and valproic acid on autism-like behavior in rats.","authors":"Maha K Alaskar, Mona Alonazi, Abir Ben Bacha, Abdulaziz M Alamri, Sameera Abuaish, Hisham S Aloudah, Mohammed Fahad Alahmed, Ahmad Tayseer AlMnaizel, Afaf K El-Ansary","doi":"10.1515/tnsci-2025-0402","DOIUrl":"10.1515/tnsci-2025-0402","url":null,"abstract":"<p><strong>Objectives: </strong>The present study aimed to evaluate the behavioral consequences of maternal immune activation (MIA) induced by lipopolysaccharide (LPS), in comparison to valproic acid (VPA), a widely used and reliable inducer of autism-like features in rats when administered during prenatal development. At the behavioral level, we further assessed the potential ameliorative effects of a standardized polyphenol-rich extract derived from the leaves of <i>Cynara cardunculus</i> L. (artichoke), used as a prebiotic - either independently or in combination with a probiotic mixture and/or omega-3 (ω3) fatty acids.</p><p><strong>Methods: </strong>Wistar albino rats prenatally exposed to LPS or VPA were evaluated for social behavior using the three-chamber social interaction test. Beginning at 7 days of age, male rat pups received specific doses of the artichoke as prebiotic (AR), probiotics (Pro), and ω3 supplements, depending on group assignment. A total of 54 neonatal male rats were divided into nine experimental groups: (1) Control group: received normal saline; (2) VPA-0 group: prenatally exposed to VPA only; (3) VPA-AR group: prenatally exposed to VPA, postnatally treated with AR; (4) VPA-AR.Pro group: prenatally exposed to VPA, postnatally treated with AR + Pro; (5) VPA.AR-AR group: received AR during gestation (protectively), and postnatal AR after VPA exposure; (6) LPS-0 group: prenatally exposed to LPS only; (7) LPS-AR group: prenatally exposed to LPS, postnatally treated with AR; (8) LPS-AR.Pro.ω3 group: prenatally exposed to LPS, postnatally treated with AR + Pro + ω3; (9) LPS.AR-AR group: received AR during gestation (protectively), and postnatal AR after LPS exposure.</p><p><strong>Results: </strong>LPS and prenatal VPA exposure significantly impair social interactions and promoting stereotypic-like behaviors. Notably, both pre- and postnatal administration of artichoke extract demonstrated significant potential in improving these behavioral deficits. MIA and prenatal VPA exposure have detrimental effects on neurobehavioral development, particularly impairing social interactions and promoting stereotypic-like behaviors consistent with ASD.</p><p><strong>Conclusions: </strong>These results provide evidence for the beneficial role of artichoke-derived prebiotics, alone or in combination with probiotics and ω3, in improving ASD-like symptoms in rodent models of autism.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250402"},"PeriodicalIF":2.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Limitations of standard memory assessments in breast cancer survivors.","authors":"Meenakshie Bradley-Garcia, Annick F N Tanguay, Gabriela Haddad, Adelaide Jensen, Melanie J Sekeres","doi":"10.1515/tnsci-2025-0401","DOIUrl":"10.1515/tnsci-2025-0401","url":null,"abstract":"<p><strong>Objectives: </strong>Breast cancer is the most commonly diagnosed cancer in women worldwide, and treatments like chemotherapy are often linked to post-treatment cognitive impairments, including memory deficits. Standardized episodic memory tests may fail to capture the nuanced, real-world aspects of memory, potentially underestimating impairments in cancer survivors. This study seeks to investigate the impact of cancer treatment on episodic memory in breast cancer survivors (BCS) by comparing standard cognitive measures with ecologically valid measures of naturalistic memory, which may capture the subtle memory impairments.</p><p><strong>Methods: </strong>BCS at least 6 months post-treatment (n=45) and non-cancer control (NC; n=43), aged 30 to 65, completed two cognitive tasks to assess episodic memory (Taler Stories and Verbal Paired Associates, VPA) and two questionnaires to assess perceived cognitive workload (National Aeronautics and Space Administration Task Load Index) and perceived episodic and semantic memory abilities (Survey of Autobiographical Memory).</p><p><strong>Results: </strong>BCS recalled fewer verbatim and gist details for the Taler Stories than NC, with impairments in gist memory persisting during delayed recall. However, no memory deficits were evident on the VPA task in BCS compared to NC. BCS reported greater cognitive effort during the story recall tasks, but no group differences emerged for the VPA task. BCS also self-reported heightened subjective difficulties with episodic and semantic memory compared to NC, which was consistent with poorer performance on the Taler Stories.</p><p><strong>Conclusions: </strong>Impaired performance on complex naturalistic memory, despite similar VPA memory task performance, suggests that standard assessments may not fully capture everyday memory challenges faced by BCS.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250401"},"PeriodicalIF":2.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The activation of glial cells in the medulla visceral zone impairs synaptic plasticity and promotes inflammation and immune disorders in sepsis.","authors":"Jianjian Wang, Lizhi Wang, Weiwei Jiang, Lu Zhu, Hongbing Li","doi":"10.1515/tnsci-2025-0398","DOIUrl":"10.1515/tnsci-2025-0398","url":null,"abstract":"<p><strong>Objective: </strong>Sepsis elicits neuroinflammation in the medullary visceral zone (MVZ), which disrupts the cholinergic anti-inflammatory pathway (CAP). However, the underlying mechanisms and translational therapeutic potential remain poorly defined.</p><p><strong>Methods: </strong>Adult male Sprague-Dawley rats received either intracerebroventricular lipopolysaccharide (LPS; 25 μg/25 μL) to induce MVZ neuroinflammation model rats, or intraperitoneal LPS (6 mg/kg) to establish polymicrobial sepsis model rats. Anti-inflammation groups were involved with minocycline sucrose solution (120 mg/L) which was administered by drinking for 4 days prior to LPS challenge. CAP transection groups were undergone right cervical vagotomy 7 days before anti-inflammation interventions. Murine sepsis score (MSS), mortality rates, heart rate variability (HRV), cytokine levels in blood and medulla, systemic immunity level, and the expression levels of glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (IBA-1), CD22, tumor necrosis factor-α (TNF-α), Munc13-1, Synaptophysin (SYN), and postsynaptic density protein 95 (PSD-95) in the MVZ were measured and analyzed.</p><p><strong>Results: </strong>Both sepsis and MVZ neuroinflammation model rats showed significantly increased mortality and MSS scores, depressed HRV parameters, and upregulated expressions of GFAP, IBA-1, CD22, and TNF-α, with downregulated expressions of Munc13-1, SYN, and PSD-95 in the MVZ. Synaptic structural damage including reduced synaptic vesicles, decreased RT1.D expression on lymphocytes, increased percentages of Th17 and Treg lymphocytes, and increased serum levels of TNF-α, IL-10, and INF-γ were observed. Anti-inflammatory intervention reversed these changes in both model rats, whereas CAP transection partially abolished the anti-inflammatory benefits, confirming CAP dependence.</p><p><strong>Conclusions: </strong>Sepsis-induced MVZ neuroinflammation dismantles synaptic integrity and CAP modulation, which intensifies peripheral cytokine storm. Early central anti-inflammation repairs MVZ synaptic plasticity and reinstates vagal immunomodulation, which may provide a translational strategy to limit septic escalation.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250398"},"PeriodicalIF":2.2,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13401058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148593304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diverse roles of connexins in the neuro-vasculature in homeostasis and disease.","authors":"Valentin Delobel, Nafiisha Genet, Karen K Hirschi","doi":"10.1515/tnsci-2025-0400","DOIUrl":"10.1515/tnsci-2025-0400","url":null,"abstract":"<p><p>Significant progress has advanced our understanding of brain physiology. The brain is now recognized as an integrated network rather than a compartmentalized organ, composed of diverse cell types including neurons, glial cells, and vascular components. Communication within this neurovascular unit relies on multiple receptors, transporters, and channels. Among these, gap junction channels formed by connexin proteins play a central role by enabling direct intercellular exchange of ions, metabolites, and signaling molecules. In the healthy brain, connexins contribute to homeostatic balance and neuronal activity, whereas their dysregulation has been implicated in the pathogenesis of multiple neurological disorders. In this review, we summarize current knowledge on the physiological roles of connexins in the brain, analyze evidence from preclinical and clinical studies linking connexin dysfunction to disease, and discuss emerging therapeutic strategies targeting connexin-mediated signaling for the treatment of brain disorders.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250400"},"PeriodicalIF":2.2,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress and molecular chaperones: a dynamic crosstalk in neurodegenerative disorders.","authors":"Leila Noori, Yousef Mohamadi, Francesco Cappello, Federica Scalia","doi":"10.1515/tnsci-2025-0397","DOIUrl":"10.1515/tnsci-2025-0397","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDs), such as Alzheimer's disease, Parkinson's disease, and Huntington's disease are discussed as representative examples of conditions in which oxidative stress and proteostasis imbalance contribute to progressive neuronal dysfunction. Oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is widely recognized as a key contributor to ND pathogenesis. Excessive ROS disrupt cellular homeostasis and promotes protein misfolding and aggregation, thereby compromising the proteostasis network. In response to this stress, molecular chaperones, including members of heat shock protein (Hsp) family, play a crucial protective role by maintaining protein folding integrity and preventing toxic aggregation. Furthermore, mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) serve as carriers of bioactive molecules, including antioxidants and molecular chaperones, offering a unique mechanism to restore cellular homeostasis. This review explores the interplay between oxidative stress and molecular chaperones in the pathogenesis of NDs and highlights the emerging therapeutic potential of MSC-EVs as modulators of oxidative and proteostatic imbalance.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250397"},"PeriodicalIF":2.2,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13293329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148332998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effects of Ershiwuwei Shanhu pills on APP/PS1 mice through antioxidant enhancement, anti-apoptosis, and MAPK pathway regulation.","authors":"Ning Li, Xiaoyuan Peng, Wei Xiong, Ce Yang, Wenxiang Wang","doi":"10.1515/tnsci-2025-0396","DOIUrl":"10.1515/tnsci-2025-0396","url":null,"abstract":"<p><strong>Objectives: </strong>Alzheimer's disease (AD) involves cognitive impairment, neuronal degeneration, oxidative imbalance, and abnormal MAPK signaling. This study investigated the protective effects of Ershiwuwei Shanhu Pills (ESP) on cognition, oxidative stress, neuronal apoptosis, and MAPK pathway regulation in APP/PS1 mice.</p><p><strong>Methods: </strong>Sixty mice were used, including 50 APP/PS1 transgenic mice randomly assigned to five groups: untreated AD model, donepezil (0.5 mg/kg), and low- (100 mg/kg), medium- (200 mg/kg), or high-dose (400 mg/kg) ESP. Ten wild-type C57BL/6J mice served as normal controls. All treatments were administered orally for 60 days. Cognitive performance was assessed by the Morris water maze. Hippocampal pathology and apoptosis were evaluated by histology and TUNEL staining, while oxidative stress markers, AD-related proteins, and MAPK phosphorylation were measured via ELISA and Western blot.</p><p><strong>Results: </strong>ESP treatment improved learning and memory performance, reduced hippocampal neuronal damage, and decreased neuronal apoptosis. Antioxidant enzyme activities (SOD, CAT, GSH, GSH-PX) increased, whereas MDA and GSSG levels decreased. Circulating Aβ1-40, Aβ1-42, TAU181, and γ-secretase levels were reduced. ESP also downregulated phosphorylation of JNK, ERK, and p38. The medium-dose group showed therapeutic effects comparable to donepezil.</p><p><strong>Conclusions: </strong>ESP exerts neuroprotective effects in APP/PS1 mice by alleviating oxidative stress, inhibiting neuronal apoptosis, and modulating MAPK signaling. These findings suggest ESP as a promising multi-target therapeutic strategy for AD.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250396"},"PeriodicalIF":2.2,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13285841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148309439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of FTO on PDCD5 mRNA stability to mediate neuron apoptosis in rats with hypoxic-ischemic brain damage.","authors":"Taiyong Yin, Minshu Zou, Dali Liu, Cui Shao, Shuangshuang Li, Hui Yuan, Hongtao Xu","doi":"10.1515/tnsci-2025-0394","DOIUrl":"10.1515/tnsci-2025-0394","url":null,"abstract":"<p><strong>Objectives: </strong>This study explored the mechanism of FTO in regulating neuron apoptosis in hypoxic-ischemic brain damage (HIBD) models via PDCD5.</p><p><strong>Methods: </strong>Neonatal SD rats were treated by unilateral common carotid artery ligation to establish HIBD model, while primary hippocampal neurons were induced by oxygen-glucose deprivation (OGD) to mimic the <i>in vitro</i> model. The expression levels of FTO and PDCD5 mRNA and proteins were assessed by qRT-PCR and Western blot, respectively. Cell apoptosis was evaluated by CCK-8 assay and flow cytometry. Furthermore, cerebral infarct area and neuronal damage in HIBD rats were determined by TTC and Nissl stainings, whereas apoptosis in brain tissue was examined by TUNEL staining. MeRIP assay was performed to detect the levels of m6A modification, and RIP assay to confirm their binding relationship.</p><p><strong>Results: </strong>HIBD rats had decreased FTO expression and elevated PDCD5 expression, accompanied by increased cerebral infarction and apoptosis. Overexpression of FTO inhibited neuronal apoptosis and alleviated HIBD progression. Additionally, knockdown of PDCD5 suppressed OGD-induced neuronal apoptosis in OGD-induced primary hippocampal neurons, while such effect was nullified by overexpression of FTO. FTO interacted with PDCD5 to influence the m6A modification level of PTBP1 and subsequently decrease its mRNA stability.</p><p><strong>Conclusions: </strong>Down-regulation of FTO expression in HIBD reduces the degradation of M6A-modified PDCD5 mRNA, thereby increasing PDCD5 protein expression. This elevation in PDCD5 promotes neuronal apoptosis, which exacerbates the progression of HIBD.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250394"},"PeriodicalIF":2.2,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13241177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148206207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research advances on estrogen deficiency leading to depression.","authors":"Chunjiao Wang, Yanfen Chang, Hui Sheng","doi":"10.1515/tnsci-2025-0399","DOIUrl":"10.1515/tnsci-2025-0399","url":null,"abstract":"<p><p>Depression is a debilitating mental disorder with a significantly higher prevalence in women, particularly during periods of hormonal fluctuation such as perimenopause, postpartum, and postmenopause. Estrogen, especially 17β-estradiol (E₂), serves as a crucial neuroactive steroid that regulates mood, cognition, and neural homeostasis through nuclear and membrane-associated receptors. Accumulating evidence suggests that estrogen deficiency contributes to the pathogenesis of depression via multiple interconnected mechanisms, including dysregulation of monoamine neurotransmission, hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, decreased brain-derived neurotrophic factor (BDNF) expression, impaired mitochondrial function and bioenergetics, neuroinflammation mediated by glial cells, and disruption of gut-brain axis communication. These alterations collectively lead to synaptic dysfunction, reduced neuroplasticity, and increased neuronal vulnerability. Therapeutic strategies such as estrogen replacement therapy (ERT), selective estrogen receptor modulators (SERMs), and receptor-specific agonists show promising antidepressant effects, particularly when administered during critical windows of hypoestrogenism. This review systematically elaborates the pathophysiological mechanisms underlying estrogen deficiency-induced depression and discusses recent advances in estrogen-based therapeutics, highlighting future directions for targeted and personalized treatment approaches.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250399"},"PeriodicalIF":2.2,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rodents' episodic-like memory: concepts, ageing, neurodegeneration, future.","authors":"Andressa Gabriela Soliani, Beatriz Gangale Muratori, Jessica Santos Baptista, Suzete Maria Cerutti","doi":"10.1515/tnsci-2025-0392","DOIUrl":"10.1515/tnsci-2025-0392","url":null,"abstract":"<p><p>Episodic memory (EM), traditionally defined as the conscious recollection of <i>what, where</i>, and <i>when</i> events occurred, was long considered uniquely human due to its reliance on autonoetic awareness. However, behavioural criteria allow memory assessment based on observable features, enabling the study of EM-related processes in non-human species and leading to the concept of episodic-like memory (ELM) in animal models. We review conceptual advances and methodological challenges in ELM research, focusing on rodent models that provide mechanistic insights into neural circuits and molecular pathways supporting memory formation and persistence. Converging evidence highlights the role of hippocampal-prefrontal networks in integrating spatial, temporal, and emotional dimensions of experience. We also discuss data from our laboratory, which provides evidence for cellular and synaptic mechanisms, such as tagging-and-capture, ensemble allocation, and reactivation, that contribute to memory linking and consolidation in the fear-based ELM paradigm. These findings indicate that novelty-dependent recruitment of neuronal ensembles in the dorsal CA1 is impaired during ageing, leading to deficits in the persistence of weak experiences. Additionally, studies using cholinergic hypofunction models, a hallmark of late-onset Alzheimer's disease (LOAD), reveal severe impairments in object recognition, spatial location, and integrated ELM, partially reversed by pharmacological interventions. Collectively, these data emphasise the translational relevance of ELM paradigms for modelling age-related memory decline and neurodegeneration. We also address open questions regarding neuromodulatory influences, sex differences, and the boundary between normal ageing and LOAD. By integrating conceptual, behavioural, and neurobiological perspectives, ELM approaches provide powerful tools for probing memory dynamics and informing therapeutic strategies.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250392"},"PeriodicalIF":2.2,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel insight into PINK1/parkin-associated autophagy implicated in Parkinson disease.","authors":"Judith Stegmüller","doi":"10.1515/tnsci-2025-0386","DOIUrl":"10.1515/tnsci-2025-0386","url":null,"abstract":"<p><p>Parkinson disease (PD) and its variants pose a dramatic burden on patients, families and society. Deciphering the mechanistic underpinnings of PD are critical goals of researchers to develop new therapeutic approaches. Among the pathways affected, autophagy draws increasing attention owing to its relationship to several genes implicated in PD and parkinsonism. This review summarizes novel insight into autophagic and in particular mitophagic processes regulated by parkin and PINK1, and how their deregulation may contribute to or cause the disease.</p>","PeriodicalId":23227,"journal":{"name":"Translational Neuroscience","volume":"17 1","pages":"20250386"},"PeriodicalIF":2.2,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}