| Literature DB >> 30605407 |
Joshua M Tublin1, Jeremy M Adelstein1, Federica Del Monte2, Colin K Combs3, Loren E Wold1,4.
Abstract
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.Entities:
Keywords: Alzheimer disease; atrial fibrillation; heart failure; inflammation; reactive oxygen species
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Year: 2019 PMID: 30605407 PMCID: PMC6319653 DOI: 10.1161/CIRCRESAHA.118.313563
Source DB: PubMed Journal: Circ Res ISSN: 0009-7330 Impact factor: 17.367