ArticleHuman molecular genetics2020
Accelerated loss of hypoxia response in zebrafish with familial Alzheimer's disease-like mutation of presenilin 1.
Article in Human molecular genetics, 2020. 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, 15 citations in OpenAlex.
- ZL006 Treatment Reduces Inflammation, Oxidative Stress, and Brain AβInternational journal of molecular sciences · 2026Article
- Knowledge About Alzheimer's Disease in Saudi Arabia.Cureus · 2023Article
- Zebrafish as a Model Organism for Studying Pathologic Mechanisms of Neurodegenerative Diseases and other Neural Disorders.Cellular and molecular neurobiology · 2023Review
- Zebrafish as a Potential Model for Neurodegenerative Diseases: A Focus on Toxic Metals Implications.International journal of molecular sciences · 2023Review
- Public Awareness of Alzheimer's Disease: A Cross-Sectional Study from Saudi Arabia.International journal of general medicine · 2022Article
- In-Frame and Frameshift Mutations in ZebrafishJournal of Alzheimer's disease reports · 2021Article
- No observed effect on brain vasculature of Alzheimer's disease-related mutations in the zebrafish presenilin 1 gene.Molecular brain · 2021Article
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
Ageing is the major risk factor for Alzheimer's disease (AD), a condition involving brain hypoxia. The majority of early-onset familial AD (EOfAD) cases involve dominant mutations in the gene PSEN1. PSEN1 null mutations do not cause EOfAD. We exploited putative hypomorphic and EOfAD-like mutations in the zebrafish psen1 gene to explore the effects of age and genotype on brain responses to acute hypoxia. Both mutations accelerate age-dependent changes in hypoxia-sensitive gene expression supporting that ageing is necessary, but insufficient, for AD occurrence. Curiously, the responses to acute hypoxia become inverted in extremely aged fish. This is associated with an apparent inability to upregulate glycolysis. Wild-type PSEN1 allele expression is reduced in post-mortem brains of human EOfAD mutation carriers (and extremely aged fish), possibly contributing to EOfAD pathogenesis. We also observed that age-dependent loss of HIF1 stabilization under hypoxia is a phenomenon conserved across vertebrate classes.
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Registered trials
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