Biogerontology最新文献

{"title":"Redox modulatory role of DJ-1 in Parkinson's disease.","authors":"Qamar A Alshammari","doi":"10.1007/s10522-025-10227-w","DOIUrl":"https://doi.org/10.1007/s10522-025-10227-w","url":null,"abstract":"<p><p>In particular, oxidative stress, generated by excessive reactive oxygen species (ROS), plays a major role in the neurodegenerative component of Parkinson's disease (PD) in aged neurons. DJ-1 (PARK7) is a key factor for maintaining redox homeostasis and modulation of mitochondrial function to preserve the cellular survival pathways. DJ-1 also plays a role in redox signaling independently of its antioxidant capacity by preventing the redox chain disulfide formation and stabilizing the master regulator of cellular antioxidant defense, Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2). In the DJ-1 or Nrf2 axis, expression of key antioxidant enzymes (glutathione peroxidase (GPx), superoxide dismutase (SOD), and heme oxygenase-1 (HO-1) in response to oxidative stress is increased, and decreased neuronal damage resulting from oxidative stress is achieved. It has been demonstrated that DJ-1 functions as an oxidative stress sensor, and mutations like L166P cause loss of antioxidant activity and increased Reactive Oxygen Species (ROS) accumulation with subsequent mitochondrial dysfunction in dopaminergic neurons. The highly conserved cysteine residue at position 106 (Cys106) of DJ-1 becomes stepwise oxidized (Cys-SOH → Cys-SO₂H → Cys-SO₃H), functioning as a redox sensor as well as redox modulator of cellular stress responses. Furthermore, by protecting against α-synuclein aggregation, DJ-1 also protects in models lacking DJ-1, whereby DJ-1 deficiency promotes protein misfolding and neurotoxicity. In addition, DJ-1 participates in regulating neuroinflammation since its diminution provokes NF-κB-mediated exacerbation of proinflammatory cytokine production, leading to neuronal death. Oxidized DJ-1 (OxiDJ-1) is generated in aging brains, particularly in the substantia nigra (SN), and is correlated with PD progression both as a biomarker for disease monitoring and diagnosis of PD early in its course. The therapeutic strategies aimed at DJ-1 include small molecular activators, protein supplementation (Tat-DJ-1, ND-13), and gene therapy aiming to restore the neuroprotective function of DJ-1. Since DJ-1 is multitasking to protect neurons from oxidative damage, mitochondrial dysfunction, and even inflammation, it remains a promising therapeutic target. This review highlights the molecular mechanisms through which DJ-1 can protect from PD and aging-related neurodegeneration and has potential utility as a biomarker or therapeutic target.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"81"},"PeriodicalIF":4.4,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural features of DNA and their potential contribution to blind mole rat (Nannospalax xanthodon) longevity.","authors":"Gamzenur Sönmez, Tuba Yağcı Gurbanov","doi":"10.1007/s10522-025-10221-2","DOIUrl":"10.1007/s10522-025-10221-2","url":null,"abstract":"<p><p>Recent research has shifted the focus from the genetic code of DNA to its structural variations, which significantly impact cancer, genetic diseases, and gene regulation. Structural changes, such as the transition from B-DNA to A-DNA, influence DNA stability and flexibility and are affected by factors like DNA methylation and sugar puckering. This study is the first to investigate the relationship between DNA conformational changes and lifespan in two rodent species. The analysis focused on long-lived Nannospalax xanthodon and shorter-lived Rattus rattus, utilizing infrared spectroscopy and principal component analysis (PCA) to examine liver DNA. Results indicated that transition from B-form to A- and Z-forms were more prevalent in N. xanthodon than in R. rattus. However, the dominant DNA conformations in both species are in B-form. Additionally, N-type sugar puckers (C3-endo conformation), associated with these DNA forms, were more prominent in N. xanthodon. In contrast, S-type sugar puckers (C2-endo conformation), characteristic of B-DNA, were found at lower levels in N. xanthodon. Furthermore, the variations in methylation-specific structural modifications of nucleobases were quantitatively assessed among these species. The study proposes a significant connection between the long lifespan of N. xanthodon, which live underground, and their unique DNA structure, offering insights into how different DNA forms, as well as the conformations of their backbone and sugar-base components, may affect longevity, highlighting potential research avenues regarding the biomolecular aspects of aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"78"},"PeriodicalIF":4.4,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708301","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 role of VEGF in vascular dementia: impact of aging and cellular senescence.","authors":"Neetu Agrawal, Muhammad Afzal, Nawaid Hussain Khan, Subbulakshmi Ganesan, Mukesh Kumari, S Sunitha, Aniruddh Dash, Kavita Goyal, Brajgopal Kushwaha, A Rekha, Mohit Rana, Haider Ali","doi":"10.1007/s10522-025-10219-w","DOIUrl":"https://doi.org/10.1007/s10522-025-10219-w","url":null,"abstract":"<p><p>Vascular Endothelial Growth Factor (VEGF) is a critical element in vascular dementia (VD) pathogenesis and therapeutic development while remaining strongly influenced by aging processes and cellular aging mechanisms. VEGF's multiple effects comprise neuroprotective functions, its role in vascular development, and its ability to regulate brain blood flow systems, all leading to cognitive preservation. The prefrontal cortex exhibits elevated VEGF gene levels, which directly matches the advancement of cognitive deficits in patients with Alzheimer's disease and VD. These patients exhibit higher VEGF levels in their CSF fluid, demonstrating that disease pathology includes multiple inseparable factors. Aging dramatically worsens VEGF regulation because endothelial dysfunction combines with chronic inflammation and oxidative stress to generate adverse vascular symptoms that include atherosclerosis and stroke. Cellular senescence convolutes these processes by causing damaging inflammatory reactions alongside impaired vascular healing abilities. The secretion of pro-inflammatory cytokines from senescent cells (SCs) disrupts VEGF signaling and produces harmful consequences for both vascular health and cognitive well-being. The neuroprotective properties of VEGF-A165a and VEGF-A165b variants demonstrate their ability to lessen β-amyloid and tau protein toxicity. The protective mechanisms of VEGF depend heavily on VEGF expression levels and receptor functionality, both of which decrease with aging. The combination of approaches that modulate VEGF signaling and SC accumulation shows potential for designing treatments against VD. People can sustain BBB functionality over a longer period through Mediterranean diet consumption together with aerobic exercise along with developing therapies, including senolytics and senomorphics, which delay neurodegenerative progression. Future investigative efforts must improve VEGF delivery methods while studying cellular senescence mechanisms and developing advanced methods to detect SC cells. A three-dimensional healthcare approach combining VEGF-targeted treatments with anti-ageing interventions and detailed diagnostic techniques shows the potential for effective VD management to achieve better patient results.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"77"},"PeriodicalIF":4.4,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of genetic/epigenetic factors and microenvironment in hematopoietic stem cell ageing.","authors":"Vahid Niazi, Benyamin Parseh, Soudeh Ghafouri-Fard","doi":"10.1007/s10522-025-10218-x","DOIUrl":"https://doi.org/10.1007/s10522-025-10218-x","url":null,"abstract":"<p><p>Hematopoietic stem cells (HSCs) ageing is a phenomenon described by reduction in self-renewal capacity, compromised homing, a bias towards myeloid differentiation, and defective reconstitution function. The molecular mechanisms of HSCs ageing have been investigated by several groups. In a broad classification, the underlying causes can be grouped into the intrinsic factors and those related to the microenvironment. Determination of the exact mechanism of HSCs ageing and detailed molecular events during its initiation and progression will help in the establishment of novel therapies for the treatment or prevention of ageing-related hematopoietic disorders. This review offers an overview of genetic and epigenetic causes of HSCs ageing. The findings of these investigations paved the way for design of novel strategies for rejuvenation of HSCs.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"76"},"PeriodicalIF":4.4,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triglycerides, high-density lipoprotein and cognitive function in middle-aged and older adults: a cross-sectional analysis.","authors":"Lanying Xie, Huanhuan Luo, Yajie Zhao, Yuqing Hao, Jie Gao, Chao Sun, Huixiu Hu","doi":"10.1007/s10522-025-10201-6","DOIUrl":"https://doi.org/10.1007/s10522-025-10201-6","url":null,"abstract":"<p><p>As China's population continues to age, addressing cognitive decline related to aging has become increasingly important. Simultaneously, rapid economic development has led to rising concerns about lipid metabolism disorders, particularly those involving blood lipids. Identifying modifiable risk factors early is critical to enhancing cognitive function in older adults. Thus, this study focuses on the relationship between triglycerides (TG), high-density lipoprotein (HDL), and cognitive performance to investigate potential mechanisms. A cross-sectional study was conducted using data from the 2015 China Health and Retirement Longitudinal Study (CHARLS) survey. Cognitive function was assessed across three domains: global cognition, episodic memory, and mental status. Fasting blood samples were analyzed for triglycerides and high-density lipoprotein (HDL) levels. The relationship between triglycerides, HDL, and cognitive function was examined using restricted cubic spline (RCS) analysis, multivariate linear regression, and mediation analysis. The analysis identifies a non-linear, inverse U-shaped relationship between triglycerides and both global cognition and episodic memory, with significant inflection points at a triglyceride (TG) level of 202.65 for global cognition and 115.04 for episodic memory. No non-linear relationship was observed between High-Density Lipoprotein (HDL) and cognitive outcomes, including global cognition, episodic memory, or mental status (p > 0.05). Linear mixed models indicate that HDL has a positive association with episodic memory, as shown by HDLQ1 (B = 0.0033, 95% CI: 0, 0.569), HDLQ2 (B = 0.039, 95% CI: 0.051, 0.594), and HDLQ3 (B = 0.033, 95% CI: 0.004, 0.556) compared to HDLQ4. A combined analysis of TG and HDL on episodic memory further demonstrated that the ''High-TG-low-HDL'' group (B = 0.036, 95% CI: 0.043, 0.578) had a significantly positive effect compared to the \"High-HDL-low-TG\" group. Mediation analysis revealed that Body Mass Index (BMI) indirectly mediated the HDL-episodic memory relationship, with a mediation effect size of 22.2%. In conclusion, this study explored the interplay between triglyceride levels, high-density lipoprotein cholesterol (HDL-C) levels, and cognitive function among middle-aged and elderly individuals in China. The findings reveal a U-shaped inverse relationship between triglyceride concentrations and cognitive ability, underscoring the need to maintain optimal triglyceride levels for cognitive health. Additionally, lower HDL levels (HDLQ1-Q3) were found to positively affect cognitive function, particularly in overall cognition and episodic memory, compared to higher HDL levels (HDLQ4). Importantly, body mass index (BMI) mediated the influence of HDL on episodic memory, with an effect size of 22.2%.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"75"},"PeriodicalIF":4.4,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The crosstalk between CNS resident glial cells and peripheral immune cells is critical for age-dependent demyelination and subsequent remyelination.","authors":"Rishika Jana, Jayasri Das Sarma","doi":"10.1007/s10522-025-10213-2","DOIUrl":"https://doi.org/10.1007/s10522-025-10213-2","url":null,"abstract":"<p><p>White-matter diseases like multiple sclerosis begin in young adulthood. Aging, being a risk factor, contributes to the progression of these diseases and makes neurological disabilities worsen. Aging causes white matter alteration due to myelin loss, axonal degeneration, and hyperintensities, resulting in cognitive impairment and neurological disorders. Aging also negatively affects central nervous system resident glial cells and peripheral immune cells, contributing to myelin degeneration and diminished myelin renewal process. Restoration of myelin failure with aging accelerates the progression of cognitive decline. This review will mainly focus on how age-related altered functions of glial and peripheral cells will affect myelin sheath alteration and myelin restoration. This understanding can give us insights into the underlying mechanisms of demyelination and failure of remyelination with aging concerning altered glial and peripheral immune cell function and their crosstalk. Also, we will explain the therapeutic strategies to enhance the remyelination process of an aging brain to improve the cognitive health of an aging person.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"74"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinguishing the intrinsic and extrinsic causes of changes in human mortality by examining life-table aging rate (LAR) trajectories through the lens of generalized Gompertz-Makeham law.","authors":"A Golubev","doi":"10.1007/s10522-025-10210-5","DOIUrl":"https://doi.org/10.1007/s10522-025-10210-5","url":null,"abstract":"<p><p>To check whether the reported waves of age-dependent changes in multiomics patterns in humans influence age-specific mortality, life-table aging rate (LAR) trajectories derived from Human Morality Database (HMD) data were modeled based on assumptions inherent in a generalized Gompertz-Makeham Law (gGML). The gGML implies that any changes in resistance to causes of death (CoD) and in exposure to CoD are translated into changes in mortality in an exponential and a linear way, respectively. Modeling suggests that undulations of LAR trajectories derived from HMD data on countries where life expectancy (LE) is above 83 years do not align with the reported waves of multiomics changes and are rather associated with changes in the exposure to CoD. As far as the exposure may be modifiable, it may be inferred from modeling that the contribution of the modifiable CoD to the total mortality is almost 100% at 25 years and reaches zero after ca. 90 years, which is no surprise. Unexpectedly, the contribution may increase by 20% at 55-65 years after the initial decrease, which reaches 30 to 70% at about 40 years. Reasons to revise approaches to attributing mortality to different CoD are discussed. Gains in LE possible upon eliminating all modifiable CoD are estimated. In the countries where LE currently exceeds 83 years, the estimates are 2.9-5.7 years for men and 1.2-2.5 for women. Thus, human LE may approach but hardly can ever exceed 90 years.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"71"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modelling orexinergic system in ageing in the African turquoise killifish.","authors":"Maria Raggio, Ivan Conte, Paolo de Girolamo, Livia D'Angelo","doi":"10.1007/s10522-025-10214-1","DOIUrl":"10.1007/s10522-025-10214-1","url":null,"abstract":"<p><p>The orexinergic system is anatomically and functionally conserved in almost all vertebrates, and the role in healthy ageing and age-associated diseases has been studied in mammals. Here, we review the main findings on the age-related regulation of orexinergic system in mammals, including human patients and highlights how the fish Nothobranchius furzeri serves as an exceptional model to spearhead research and unravel the intricate mechanisms underlying orexinergic regulation during ageing. The ageing brain of this teleost is characterized by the presence of neurodegenerative processes similar to those associated with human pathologies rather than those of healthy ageing. We present an in-depth summary and discussion on the groundbreaking advances in understanding the neuroanatomical organization of the orexinergic system, its pivotal role in mammalian and fish models, and its profound involvement in healthy ageing and age-associated diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"72"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630150","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":"Chrysin alleviates the impeded neurogenesis in accelerated brain aging by D-galactose in rats.","authors":"Ram Prajit, Nataya Sritawan, Anusara Aranarochana, Apiwat Sirichoat, Wanassanun Pannangrong, Peter Wigmore, Jariya Umka Welbat","doi":"10.1007/s10522-025-10215-0","DOIUrl":"https://doi.org/10.1007/s10522-025-10215-0","url":null,"abstract":"<p><p>Aged-related cognitive impairments are associated with molecular neurodegenerations and impeded neurogenesis in the dentate gyrus (DG) of the damaged hippocampus. Neurogenesis requires activated cyclic AMP-responsive element-binding protein (CREB) pathway to enhance neuronal development, synaptic plasticity, cognition, learning and memory. Current research has reported that consecutive administration of D-galactose can accelerate brain aging by inducing oxidation and inflammation. The flavonoid chrysin has been demonstrated in medical dietary supplements and shown neuroprotective effect on impeded neurogenesis. This study aimed to clarify that chrysin preserves neurogenesis by modulating molecular pathway in accelerated brain aging induced by D-galactose. Signs of aging, processes of neurogenesis, and protein regulating neurogenesis were evaluated in male Sprague Dawley (SD) rats, which were allocated into four groups: vehicle rats, accelerated aging rats treated with D-galactose, normal rats receiving chrysin, and cotreated rats receiving both D-galactose and chrysin. Aging signs showed only a subsidence in volume of the granular cell layer (GCL) after consecutive administration of D-galactose. Cell proliferation, neurogenic niches, and protein regulating proliferation were downregulated in the accelerated aging rats. Likewise, cell survivals and proteins related to CREB pathway were depleted in rats receiving D-galactose. Nevertheless, rats cotreated with chrysin maintained in all parameters that were adversely affected by D-galactose. In conclusion, chrysin could alleviate the disruption of molecular regulation of neurogenesis in accelerated brain aging induced by D-galactose.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"70"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammation increases in old and oldest-old rats except for dura mater meningeal tissue with significant gender differences: a translational perspective.","authors":"Leonardo Biscetti, Salvatore Vaiasicca, Belinda Giorgetti, Paola Sarchielli, Fiorenza Orlando, Alessandro Di Rienzo, Erika Carrassi, Mirko Di Rosa, Serena Marcozzi, Tiziana Casoli, Giuseppe Pelliccioni","doi":"10.1007/s10522-025-10212-3","DOIUrl":"https://doi.org/10.1007/s10522-025-10212-3","url":null,"abstract":"<p><p>Neuroinflammaging is the nervous system version of inflammaging, the low-grade inflammation that develops with advanced age, aside from active disease or infection. Despite neuroinflammaging has been widely investigated, some important issues still need to be resolved such as the analysis of the extremely old subjects and the evaluation of specific brain areas. On this background, we conducted a study to analyze expression of inflammatory and anti-inflammatory genes in Wistar rats of different ages, including the oldest-old, in different brain regions. We found that pro-inflammatory mediators were generally up-regulated with age in cortex, hippocampus, and striatum, especially in the oldest-old group. Specifically, TNF-α showed an increment in expression with age in striatum, IL-1β and IFN-γ in hippocampus, and MCP-1 in cortex, hippocampus and striatum. Conversely, CX3CL1 and NOS2 showed a significant reduction of expression in the cortex of the oldest-old group. A different situation was observed in dura mater where TNF-α, IL-6, IL-1β, CX3CL1, and MCP-1 expression decreased in the older groups in comparison with the younger groups. With age the anti-inflammatory cytokines IL-4 and IL-10 were down-regulated in cortex, and TGF-β1 in dura mater, while IL-4 was up-regulated in the oldest-old group in hippocampus. Finally, we observed that female brains underwent an age-related increase of pro-inflammatory cytokines expression compared to males, except for striatum, and a general down-regulation of anti-inflammatory cytokines within each age group. Protein validation of selected factors by ELISA tests supported the observed changes. These data may represent a basis for future research about the neurobiology of aging, in particular in the neurodegenerative disorder framework.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"73"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}