The Alzheimer’s Disease Amyloid-Beta Hypothesis in Cardiovascular Aging and Disease
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Aging-related cellular and molecular processes including low-grade inflammation are major players in the pathogenesis of cardiovascular disease (CVD) and Alzheimer's disease (AD). Epidemiological studies report an independent interaction between the development of dementia and the incidence of CVD in several populations, suggesting the presence of overlapping molecular mechanisms. Accumulating experimental and clinical evidence suggests that amyloid-beta (Aβ) peptides may function as a link among aging, CVD, and AD. Aging-related vascular and cardiac deposition of Αβ induces tissue inflammation and organ dysfunction, both important components of the Alzheimer's disease amyloid hypothesis. In this review, the authors describe the determinants of Aβ metabolism, summarize the effects of Aβ on atherothrombosis and cardiac dysfunction, discuss the clinical value of Αβ1-40 in CVD prognosis and patient risk stratification, and present the therapeutic interventions that may alter Aβ metabolism in humans.
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APP/PS1-F5KO mice have higher cortical soluble Aβ−40 levels than APP/PS1-WT mice, with no such difference in hippocampus.
“Interestingly, in the cortex, APP/PS1-F5KO showed significantly higher levels of soluble Aβ−40, which contributes to plaque formation and more dysfunctional vascular integrity 54,55, compared to APP/PS1-WT However, the hippocampus did not present such differences (Extended Data Fig. 5a, b).”
From Exercise hormone irisin is a critical regulator of cognitive function (2021) · cites this paper as [55]
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- Authors
- Stakos, D. A., Stamatelopoulos, K., Bampatsias, D., Sachse, M., Zormpas, E., Vlachogiannis, N. I., Tual-Chalot, S., & Stellos, K.
- Affiliations
- Democritus University of Thrace (GR)
- National and Kapodistrian University of Athens (GR)
- Goethe University Frankfurt (DE)
- Newcastle University (GB)
- Newcastle upon Tyne Hospitals NHS Foundation Trust (GB)
- Corresponding author
- Stellos, Konstantinos
- ORCID
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2020-03
- Volume
- 75
- Issue
- 8
- Pages
- 952-967
- ISSN
- 0735-1097 (ISSN-L)
- PMC
- PMC7042886
- OpenAlex
- W3007333794
- Cited by
- 188
- References
- 121
- Citations by year
- 2026: 16 · 2025: 45 · 2024: 32 · 2023: 35 · 2022: 25 · 2021: 23 · 2020: 12
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- European Research Council
- Deutsche Forschungsgemeinschaft (75732319, SFB834)
- 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, amyloid-beta, amyloid hypothesis, cardiovascular aging, cardiovascular disease, dementia, low-grade inflammation, atherothrombosis, cardiac dysfunction, amyloid-beta metabolism, Aβ40, risk stratification, Alzheimer's disease therapeutics
- MeSH terms
- Aging, Alzheimer Disease, Animals, Cardiovascular Diseases, Humans, Mortality, Amyloid beta-Peptides, Risk Assessment
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