Neural stem cells (NSCs) generate new neurons throughout life in the mammalian hippocampus. Advancing age leads to a decline in neurogenesis, which is associated with impaired cognition. The cellular mechanisms causing reduced neurogenesis with advancing age remain largely unknown. We genetically labeled NSCs through conditional recombination driven by the regulatory elements of the stem-cell-expressed gene GLI family zinc finger 1 (Gli1) and used chronic intravital imaging to follow individual NSCs and their daughter cells over months within their hippocampal niche. We show that aging affects multiple steps, from cell cycle entry of quiescent NSCs to determination of the number of surviving cells, ultimately causing reduced clonal output of individual NSCs. Thus, we here define the developmental stages that may be targeted to enhance neurogenesis with the aim of maintaining hippocampal plasticity with advancing age.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10154232 | PMC |
| http://dx.doi.org/10.1038/s43587-023-00370-9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Shift work schedules alter immune cell regulation and accelerate cognitive impairment during aging.
J Neuroinflammation
January 2025
Department of Neuroscience and Experimental Therapeutics, School of Medicine, Texas A&M Health Science Center, Bryan, TX, 77807-3260, USA.
Background: Disturbances of the sleep-wake cycle and other circadian rhythms typically precede the age-related deficits in learning and memory, suggesting that these alterations in circadian timekeeping may contribute to the progressive cognitive decline during aging. The present study examined the role of immune cell activation and inflammation in the link between circadian rhythm dysregulation and cognitive impairment in aging.
Methods: C57Bl/6J mice were exposed to shifted light-dark (LD) cycles (12 h advance/5d) during early adulthood (from ≈ 4-6mo) or continuously to a "fixed" LD12:12 schedule.
Subgroups of cognitive impairments in schizophrenia characterized by executive function and their morphological features: a latent profile analysis study.
BMC Med
January 2025
Department of Psychiatry, National Clinical Research Center for Mental Disorders, and National Center for Mental Disorders, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Background: The heterogeneity of cognitive impairments in schizophrenia has been widely observed. However, reliable cognitive boundaries to differentiate the subgroups remain elusive. The key challenge for cognitive subtyping is applying an integrated and standardized cognitive assessment and understanding the subgroup-specific neurobiological mechanisms.
View Article and Find Full Text PDFDevelopment and validation of a five-year cardiovascular risk assessment tool for Asian adults aged 75 years and older.
BMC Geriatr
January 2025
Graduate Institute of Clinical Pharmacy, College of Medicine, National Taiwan University, No. 33, Linsen S. Rd., Zhongzheng Dist., Taipei, 100025, Taiwan.
Background: To identify cardiovascular (CV) risk factors in Asian elderly aged 75 years and older and subsequently develop and validate a sex-specific five-year CV risk assessment tool for this population.
Methods: This study included 12,174 patients aged ≥ 75 years without a prior history of cardiovascular disease at a single hospital in Taiwan. Electronic health records were linked to the National Health Insurance Research Database and the National Death Registry to ensure comprehensive health information.
EBP1 potentiates amyloid β pathology by regulating γ-secretase.
Nat Aging
January 2025
Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea.
The abnormal deposition of amyloid β (Aβ), produced by proteolytic cleavage events of amyloid precursor protein involving the protease γ-secretase and subsequent polymerization into amyloid plaques, plays a key role in the neuropathology of Alzheimer's disease (AD). Here we show that ErbB3 binding protein 1 (EBP1)/proliferation-associated 2G4 (PA2G4) interacts with presenilin, a catalytic subunit of γ-secretase, inhibiting Aβ production. Mice lacking forebrain Ebp1/Pa2g4 recapitulate the representative phenotypes of late-onset sporadic AD, displaying an age-dependent increase in Aβ deposition, amyloid plaques and cognitive dysfunction.
View Article and Find Full Text PDFQuantitative magnetization transfer and g-ratio imaging of white matter myelin in early psychotic spectrum disorders.
Mol Psychiatry
January 2025
Department of Radiology, NYU Grossman School of Medicine, New York, NY, USA.
Myelin abnormalities in white matter have been implicated in the pathophysiology of psychotic spectrum disorders (PSD), which are characterized by brain dysconnectivity as a core feature. Among evidence from in vivo MRI studies, diffusion imaging findings have largely supported disrupted white matter integrity in PSD; however, they are not specific to myelin changes. Using a multimodal imaging approach, the current study aimed to further delineate myelin and microstructural changes in the white matter of a young PSD cohort.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!