TY - JOUR
T1 - Heart and Brain
T2 - Complex Relationships for Left Ventricular Dysfunction
AU - Daniele, Gianlorenzo
AU - DiLucia, Stephanie
AU - Masci, Pier Giorgio
AU - del Monte, Federica
N1 - Publisher Copyright:
© 2020, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2020/8/1
Y1 - 2020/8/1
N2 - Purpose of Review: This review summarizes the evidence for the established vascular/hypoperfusion model and explores the new hypothesis that configures the heart/brain axis as an organ system where similar pathogenic mechanisms exploit physiological and pathological changes. Recent Findings: Although associated by common risk factors, similar epidemiological stratification and common triggers (including inflammation, oxidative stress, and hypoxia), heart failure and Alzheimer’s disease have been, for long time, viewed as pathogenically separate illnesses. The silos began to be broken down with the awareness that vascular dysfunction, and loss of cardiac perfusion pump power, trigger biochemical changes, contributing to the typical hallmark of Alzheimer’s disease (AD)—the accumulation of Aβ plaques and hyperphosphorylated Tau tangles. Compromised blood flow to the brain becomes the paradigm for the “heart-to-head” connection. Compelling evidence of common genetic variants, biochemical characteristics, and the accumulation of Aβ outside the brain suggests a common pathogenesis for heart failure (HF) and AD. These new findings represent just the beginning of the understanding the complex connection between AD and HF requiring further studies and interdisciplinary approaches. Summary: Altogether, the current evidence briefly summarized in this review, highlight a closer and complex relationship between heart failure and Alzheimer’s that goes beyond the vascular/perfusion hypothesis. Genetic and biochemical evidence begin to suggest common pathogenic mechanisms between the two diseases involving a systemic defect in the folding of protein or a seeding at distance of the misfolded proteins from one organ to the other.
AB - Purpose of Review: This review summarizes the evidence for the established vascular/hypoperfusion model and explores the new hypothesis that configures the heart/brain axis as an organ system where similar pathogenic mechanisms exploit physiological and pathological changes. Recent Findings: Although associated by common risk factors, similar epidemiological stratification and common triggers (including inflammation, oxidative stress, and hypoxia), heart failure and Alzheimer’s disease have been, for long time, viewed as pathogenically separate illnesses. The silos began to be broken down with the awareness that vascular dysfunction, and loss of cardiac perfusion pump power, trigger biochemical changes, contributing to the typical hallmark of Alzheimer’s disease (AD)—the accumulation of Aβ plaques and hyperphosphorylated Tau tangles. Compromised blood flow to the brain becomes the paradigm for the “heart-to-head” connection. Compelling evidence of common genetic variants, biochemical characteristics, and the accumulation of Aβ outside the brain suggests a common pathogenesis for heart failure (HF) and AD. These new findings represent just the beginning of the understanding the complex connection between AD and HF requiring further studies and interdisciplinary approaches. Summary: Altogether, the current evidence briefly summarized in this review, highlight a closer and complex relationship between heart failure and Alzheimer’s that goes beyond the vascular/perfusion hypothesis. Genetic and biochemical evidence begin to suggest common pathogenic mechanisms between the two diseases involving a systemic defect in the folding of protein or a seeding at distance of the misfolded proteins from one organ to the other.
KW - Alzheimer’s disease
KW - Aβ
KW - Cardiomyopathy
KW - Heart failure
KW - Protein folding
KW - Vascular dementia
UR - http://www.scopus.com/inward/record.url?scp=85086784864&partnerID=8YFLogxK
U2 - 10.1007/s11886-020-01318-w
DO - 10.1007/s11886-020-01318-w
M3 - Review article
C2 - 32577917
AN - SCOPUS:85086784864
SN - 1523-3782
VL - 22
JO - Current cardiology reports
JF - Current cardiology reports
IS - 8
M1 - 72
ER -
