In a somewhat narrow diagnostic lens, Alzheimer’s Disease (AD) has been considered a brain specific disease characterized by the presence of 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 (HF), coronary artery disease (CAD), atrial fibrillation (AF), 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. β amyloid 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 (iDCM) 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 HF and AD. Herein, we provide an overview of the cardiovascular links to Alzheimer’s disease.

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