The association between PGC-1α and Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is a neurodegenerative disorder and its reported pathophysiological features in the brain include the deposition of amyloid beta peptide, chronic inflammation, and cognitive impairment. The incidence of AD is increasing worldwide and researchers have studied various aspects of AD pathophysiology in order to improve our understanding of the disease. Thus far, the onset mechanisms and means of preventing AD are completely unknown. Peroxisome proliferator-activated receptor-γ coactivator (PGC-1α) is a protein related to various cellular mechanisms that lead to the alteration of downstream gene regulation. It has been reported that PGC-1α could protect cells against oxidative stress and reduce mitochondrial dysfunction. Moreover, it has been demonstrated to have a regulatory role in inflammatory signaling and insulin sensitivity related to cognitive function. Here, we present further evidence of the involvement of PGC-1α in AD pathogenesis. Clarifying the relationship between PGC-1α and AD pathology might highlight PGC-1α as a possible target for therapeutic intervention in AD.
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PPARGC1A/PGC-1α regulates mitochondrial function and cellular responses to oxidative stress and has been implicated in AD-associated metabolic dysfunction.
“PPARGC1A/PGC-1α regulates mitochondrial function and cellular responses to oxidative stress and has been implicated in AD-associated metabolic dysfunction (Sweeney and Song, 2016).”
From Isogenic human stem cell models reveal mutation-dependent protective mechanisms of APOE3 Christchurch (2026) · cites this paper as Sweeney and Song, 2016
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- Authors
- Sweeney, G., & Song, J.
- Affiliations
- York University (CA)
- Yonsei University (KR)
- Corresponding author
- Song, Juhyun
- Venue
- Anatomy & Cell Biology
- Publisher
- Korean Association of Anatomists
- Published
- 2016
- Volume
- 49
- Issue
- 1
- Pages
- 1
- ISSN
- 2093-3665 (ISSN-L)
- 2093-3673
- PMC
- PMC4819073
- OpenAlex
- W2330994131
- Cited by
- 93
- References
- 11
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 8 · 2023: 5 · 2022: 9 · 2021: 12 · 2020: 22 · 2019: 7 · 2018: 10 · 2017: 6 · 2016: 2
- FWCI
- 0.98
- Type
- journal article
- Language
- en
- Update notices
- erratum (2016-06-24)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Anatomy & Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- PGC-1α, Alzheimer's disease, amyloid-beta, neuroinflammation, oxidative stress, mitochondrial dysfunction, insulin sensitivity, cognitive impairment, gene expression regulation, therapeutic target
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