ArticleAging cell2024
Activation of the hypoxia response in the aging cerebrovasculature protects males against cognitive impairment.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- "Morphological, Functional, and Molecular Progression of Blood-Brain Barrier Dysfunction in Alzheimer's Disease".Journal of molecular neuroscience : MN · 2026Review
- ERα Agonist Protects Aged Female Mice From Sevoflurane Neurotoxicity via PTEN Nuclear Translocation.CNS neuroscience & therapeutics · 2026Article
- Single-Nucleus Profiling Reveals a BBB Senescence Unit Driving AD Pathology in Human Brain.Molecular neurobiology · 2026Article
- Dysfunction of the neurovascular unit as a temporal driver in Alzheimer's pathogenesis.Translational neurodegeneration · 2026Review
- Sex-Specific Biological Aging-Related Lipidomic Profiles Mediate the Impact of Urinary Polycyclic Aromatic Hydrocarbon Exposures on Cognitive Function in Healthy Older Adults.Environment & health (Washington, D.C.) · 2026Article
- HSP72-AMPK axis mitigates hypoxia-induced cellular senescence to promote colorectal cancer development.Molecular and cellular biochemistry · 2026Article
- Integrative Transcriptomic Analysis Decodes the Interplay Between Aging, Senescence, and Cancer.Cancer science · 2025Article
- Activation of the hypoxia response in the aging cerebrovasculature protects males against cognitive impairment.Aging cell · 2024Article
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Authors and funding
13 authors.
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Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder with a distinct sex bias. Age-related vascular alterations, a hallmark of AD onset and progression, are consistently associated with sexual dimorphism. Here, we conducted an integrative meta-analysis of 335,803 single-nucleus transcriptomes and 667 bulk transcriptomes from the vascular system in AD and normal aging to address the underlying sex-dependent vascular aging in AD. All vascular cell types in male AD patients exhibited an activated hypoxia response and downstream signaling pathways including angiogenesis. The female AD vasculature is characterized by increased antigen presentation and decreased angiogenesis. We further confirmed that these sex-biased alterations in the cerebral vascular emerged and were primarily determined in the early stages of AD. Sex-stratified analysis of normal vascular aging revealed that angiogenesis and various stress-response genes were downregulated concurrently with female aging. Conversely, the hypoxia response increased steadily in males upon aging. An investigation of upstream driver transcription factors (TFs) revealed that altered communication between estrogen receptor alpha (ESR1) and hypoxia induced factors during menopause contributes to the inhibition of angiogenesis during normal female vascular aging. Additionally, inhibition of CREB1, a TF that targets estrogen, is also related to female AD. Overall, our study revealed a distinct cerebral vascular profile in females and males, and revealed novel targets for precision medicine therapy for AD.
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