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Hypoxia‐inducible factors as neuroprotective agent in Alzheimer's disease
Abstract
Summary: Beta amyloid (Aβ)‐42 peptide and phosphorylated tau protein have been demonstrated as the pathological hallmarks of Alzheimer's disease (AD). A gradual decline of oxygen and glucose supply to the brain during aging or hypoxia was manifested as a contributing factor to hypometabolism. The brain regions susceptible to hypometabolism are the hippocampus, entorhinal cortex and cognition‐associated neocortical regions like parietal, temporal and frontal cortex. In AD patients, the brain regions with hypometabolism can trigger overexpression of amyloid precursor protein and decrease the clearance of Aβ. Aβ and hypoxia can evoke inflammation, oxidative stress and finally neuronal cell death. Among the transcription factors involved in the compensatory mechanism, hypoxia‐inducible factor‐1 alpha (HIF‐1α) has a major role in the cellular adaptation by inducing the expression of several proteins, including vascular endothelial growth factor, erythropoietin and inducible nitric oxide synthase. Therefore, maintaining the HIF‐1α level by inhibiting the prolyl 4‐hydroxylase was effective to attenuate the nerve damage during hypoxia and postpone the incidence of AD. Agents such as iron chelators, and heavy metals like cobalt and nickel were demonstrated to be effective in maintaining the HIF‐1α level in the nerve. This review article discusses the possible role of HIF‐1α as a neuroprotector in AD and the future perspectives.
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“reduced vascular diameters and increased capillary densities [123] have been documented in aged individuals and AD [124]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [124]
In the citing paper
“reduced vascular diameters and increased capillary densities [123] have been documented in aged individuals and AD [124]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [124]
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Metadata
- Authors
- Ashok, B. S., Ajith, T. A., & Sivanesan, S.
- Affiliations
- Sri Ramachandra Institute of Higher Education and Research (IN)
- Amala Institute of Medical Sciences (IN)
- Saveetha University (IN)
- Corresponding author
- Ajith, Thekkuttuparambil Ananthanarayanan
- Sivanesan, Senthilkumar
- Venue
- Clinical and Experimental Pharmacology and Physiology
- Publisher
- Wiley
- Published
- 2017-02-14
- Volume
- 44
- Issue
- 3
- Pages
- 327-334
- ISSN
- 0305-1870 (ISSN-L)
- 1440-1681
- OpenAlex
- W2564524475
- Cited by
- 150
- References
- 100
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 31 · 2023: 11 · 2022: 15 · 2021: 35 · 2020: 13 · 2019: 14 · 2018: 9 · 2017: 6
- FWCI
- 1.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical and Experimental Pharmacology and Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- hypoxia-inducible factor-1α, Alzheimer's disease, neuroprotection, amyloid-beta, tau phosphorylation, brain hypometabolism, oxidative stress, neuroinflammation, iron chelators, cobalt, nickel, vascular endothelial growth factor, erythropoietin, inducible nitric oxide synthase
- MeSH terms
- Alzheimer Disease, Animals, Humans, Peptide Fragments, Amyloid beta-Peptides, Neuroprotective Agents, Hypoxia-Inducible Factor 1, alpha Subunit, Drug Discovery
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