Getting to the Heart of Alzheimer Disease
Open accessAbstract
In a somewhat narrow diagnostic lens, Alzheimer disease (AD) has been considered a brain-specific disease characterized by the presence of Aβ (β-amyloid) plaques and tau neural fibrillary tangles and neural inflammation; these pathologies lead to neuronal death and consequently clinical symptoms, such as memory loss, confusion, and impaired cognitive function. However, for decades, researchers have noticed a link between various cardiovascular abnormalities and AD—such as heart failure, coronary artery disease, atrial fibrillation, and vasculopathy. A considerable volume of work has pointed at this head to heart connection, focusing mainly on associations between cerebral hypoperfusion and neuronal degradation. However, new evidence of a possible systemic or metastatic profile to AD calls for further analysis of this connection. Aβ aggregations—biochemically and structurally akin to those found in the typical AD pathology—are now known to be present in the hearts of individuals with idiopathic dilated cardiomyopathy, as well as the hearts of patients with AD. These findings suggest a potential systemic profile of proteinopathies and a new hypothesis for the link between peripheral and central symptoms of heart failure and AD. Herein, we provide an overview of the cardiovascular links to Alzheimer disease.
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Cerebral ischaemia and hypoxia due to chronic brain hypoperfusion disrupt neuronal energy metabolism and lead to acidosis and oxidative stress, ultimately causing neuronal degeneration and cognitive impairment in an Aβ-independent manner.
“Furthermore, cerebral ischaemia and hypoxia due to CBH disrupt neuronal energy metabolism and lead to acidosis and oxidative stress, ultimately causing neuronal degeneration and cognitive impairment in an Aβ-independent manner.212”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [212]
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References 81 · Cited by 188
Research works printed but not linked: 4
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- Authors
- Tublin, J. M., Adelstein, J. M., del Monte, F., Combs, C. K., & Wold, L. E.
- Affiliations
- The Ohio State University (US)
- Medical University of South Carolina, Charleston (F.d.M.)
- University of North Dakota (US)
- Corresponding author
- Wold, Loren E.
- Venue
- Circulation Research
- Published
- 2019-01-04
- Volume
- 124
- Issue
- 1
- Pages
- 142-149
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC6319653
- OpenAlex
- W2906947934
- Cited by
- 188
- References
- 81
- Citations by year
- 2026: 8 · 2025: 22 · 2024: 24 · 2023: 37 · 2022: 30 · 2021: 32 · 2020: 22 · 2019: 13
- FWCI
- 2.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion, other-oa)
- Funders
- American Heart Association (17CSA33620007)
- National Institutes of Health
- National Institute on Aging (R01AG057046)
- National Heart, Lung, and Blood Institute (R01HL139348, R01HL156116)
- National Institute of Nursing Research (R01NR012618)
- National Institute of Environmental Health Sciences (R01ES019923)
- 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 › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, cardiovascular comorbidity, amyloid-beta, tau pathology, cerebral hypoperfusion, heart failure, idiopathic dilated cardiomyopathy, atrial fibrillation, coronary artery disease, vasculopathy, heart-brain interaction
- MeSH terms
- Alzheimer Disease, Animals, Brain, Cardiovascular Diseases, Cardiovascular System, Cerebrovascular Circulation, Humans, Prognosis, Risk Factors, Signal Transduction, Amyloid beta-Peptides, Reactive Oxygen Species, Oxidative Stress, Inflammation Mediators, Plaque, Amyloid
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