Sex- and brain region-specific acceleration of β-amyloidogenesis following behavioral stress in a mouse model of Alzheimer's disease
Open accessAbstract
BACKGROUND: It is hypothesized that complex interactions between multiple environmental factors and genetic factors are implicated in sporadic Alzheimer's disease (AD); however, the underlying mechanisms are poorly understood. Importantly, recent evidence reveals that expression and activity levels of the β-site APP cleaving enzyme 1 (BACE1), which initiates amyloid-β (Aβ) production, are elevated in AD brains. In this study, we investigated a molecular mechanism by which sex and stress interactions may accelerate β-amyloidogenesis and contribute to sporadic AD. RESULTS: We applied 5-day restraint stress (6 h/day) to the male and female 5XFAD transgenic mouse model of AD at the pre-pathological stage of disease, which showed little amyloid deposition under non-stressed control conditions. Exposure to the relatively brief behavioral stress increased levels of neurotoxic Aβ42 peptides, the β-secretase-cleaved C-terminal fragment (C99) and plaque burden in the hippocampus of female 5XFAD mice but not in that of male 5XFAD mice. In contrast, significant changes in the parameters of β-amyloidosis were not observed in the cerebral cortex of stressed male or female 5XFAD mice. We found that this sex- and brain region-specific acceleration of β-amyloidosis was accounted for by elevations in BACE1 and APP levels in response to adverse stress. Furthermore, not only BACE1 mRNA but also phosphorylation of the translation initiation factor eIF2α (a proposed mediator of the post-transcriptional upregulation of BACE1) was elevated in the hippocampus of stressed female 5XFAD mice. CONCLUSIONS: Our results suggest that the higher prevalence of sporadic AD in women may be attributable to the vulnerability of female brains (especially, the hippocampus) to stressful events, which alter APP processing to favor the β-amyloidogenesis through the transcriptional and translational upregulation of BACE1 combined with elevations in its substrate APP.
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Female 5XFAD mice have increased BACE1 activity, leading to increased amyloid plaque burden compared to male 5XFAD mice.
“Females also appear to have increased BACE1 activity, a β-secretase processing enzyme which cleaves pAPP and produces pathogenic Aβ fragments [40,41], ultimately leading to increased amyloid plaque burden compared to male 5XFAD mice [41,42].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [41]
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- Authors
- Devi, L., Alldred, M. J., Ginsberg, S. D., & Ohno, M.
- Affiliations
- Nathan Kline Institute for Psychiatric Research (US)
- Corresponding author
- Ohno, Masuo
- Venue
- Molecular Brain
- Published
- 2010-11-08
- Volume
- 3
- Issue
- 1
- Pages
- 34-34
- ISSN
- 1756-6606 (ISSN-L)
- PMC
- PMC2988063
- OpenAlex
- W2171661607
- Cited by
- 129
- References
- 77
- Citations by year
- 2026: 1 · 2025: 9 · 2024: 11 · 2023: 11 · 2022: 7 · 2021: 10 · 2020: 8 · 2019: 13 · 2018: 11 · 2017: 9 · 2016: 5 · 2015: 8 · 2014: 6 · 2013: 7 · 2012: 7
- FWCI
- 4.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Brain (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Alzheimer's Association (IIRG-08-91231)
- National Institutes of Health
- National Institute on Aging (P01AG014449, R01AG043375, P01AG017617)
- National Institute of Mental Health (R01MH067251)
- 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
- Alzheimer's disease, behavioral stress, restraint stress, sex differences, 5xFAD mice, BACE1, amyloid-beta 42, APP processing, eIF2α phosphorylation, hippocampus, cerebral cortex, amyloid plaques
- MeSH terms
- Alzheimer Disease, Animals, Behavior, Animal, Brain, Disease Models, Animal, Female, Humans, Male, Mice, Transgenic, Sex Factors, Stress, Psychological, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Mice, Amyloid Precursor Protein Secretases
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