Glucose metabolism, neural cell senescence and Alzheimer's disease
Open accessAbstract
Alzheimer’s disease (AD), an elderly neurodegenerative disorder with a high incidence and progressive memory decline, is one of the most expensive, lethal, and burdening diseases. To date, the pathogenesis of AD has not been fully illustrated. Emerging studies have revealed that cellular senescence and abnormal glucose metabolism in the brain are the early hallmarks of AD. Moreover, cellular senescence and glucose metabolism disturbance in the brain of AD patients may precede amyloid-β deposition or Tau protein phosphorylation. Thus, metabolic reprogramming targeting senescent microglia and astrocytes may be a novel strategy for AD intervention and treatment. Here, we recapitulate the relationships between neural cell senescence and abnormal glucose metabolism (e.g., insulin signaling, glucose and lactate metabolism) in AD. We then discuss the potential perspective of metabolic reprogramming towards an AD intervention, providing a theoretical basis for the further exploration of the pathogenesis of and therapeutic approach toward AD.
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Reduced insulin/PI3K signaling contributes to widespread proteomic synaptic and metabolic compromise in CA1/CA2, even when transcriptional changes in PI3K components are modest.
“Although CA1 and CA2 did not show the largest changes in PIK3CA transcriptionally, each exhibited pronounced proteomic evidence of downstream pathway remodeling, suggesting that reduced insulin/PI3K signaling contributes to widespread proteomic synaptic and metabolic compromise in CA1/CA2, 42 , 66 , 67 even when transcriptional changes in PI3K components are modest.”
From Disruption of hippocampal upstream regulators of mTOR and insulin pathways in Down syndrome with Alzheimer's disease neuropathology: Preliminary observations (2026) · cites this paper as [67]
Section 4.1 links impaired insulin/PI3K-AKT signaling to reduced glucose metabolism and impaired synaptic plasticity, supporting the proposed general mechanism. It does not establish proteomic compromise specifically in CA1/CA2 or relate it to modest transcriptional changes in PI3K components. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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Self-citation
- Authors
- Wang, Q., Duan, L., Li, X., Wang, Y., Guo, W., Guan, F., & Ma, S.
- Affiliations
- Zhengzhou University (CN)
- Corresponding author
- Guan, Fangxia
- Ma, Shanshan
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2022-04-14
- Volume
- 23
- Issue
- 8
- Pages
- 4351
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC9030802
- OpenAlex
- W4224072296
- Cited by
- 90
- References
- 170
- Citations by year
- 2026: 18 · 2025: 22 · 2024: 23 · 2023: 23 · 2022: 4
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (U2004201)
- Central Plains Thousand People Plan of Henan Province (204200510013)
- Henan Overseas Expertise Introduction Center for Discipline Innovation (CXJD2021002)
- The Key Science and Technology Research Project of Henan Province of China (212102310175)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, cellular senescence, glucose metabolism, metabolic reprogramming, insulin signaling, lactate metabolism, amyloid-beta deposition, tau phosphorylation, neurodegeneration
- MeSH terms
- Aged, Alzheimer Disease, Brain, Glucose, Humans, Neurons, Amyloid beta-Peptides, Cellular Senescence
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