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Aβ Amyloid Pathology Affects the Hearts of Patients With Alzheimer’s Disease

Journal of the American College of Cardiology, ISSN: 0735-1097, Vol: 68, Issue: 22, Page: 2395-2407
2016
  • 136
    Citations
  • 0
    Usage
  • 225
    Captures
  • 1
    Mentions
  • 121
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    136
    • Citation Indexes
      134
    • Patent Family Citations
      1
      • Patent Families
        1
    • Policy Citations
      1
      • Policy Citation
        1
  • Captures
    225
  • Mentions
    1
    • News Mentions
      1
      • News
        1
  • Social Media
    121
    • Shares, Likes & Comments
      121
      • Facebook
        121

Most Recent News

Aβ Amyloid Pathology Affects the Hearts of Patients With Alzheimer's Disease: Mind the Heart.

J Am Coll Cardiol. 2016 Dec 6;68(22):2395-2407. Authors: Troncone L, Luciani M, Coggins M, Wilker EH, Ho CY, Codispoti KE, Frosch MP, Kayed R, Del Monte F PubMed: 27908343 Submit Comment

Article Description

Individually, heart failure (HF) and Alzheimer’s disease (AD) are severe threats to population health, and their potential coexistence is an alarming prospect. In addition to sharing analogous epidemiological and genetic profiles, biochemical characteristics, and common triggers, the authors recently recognized common molecular and pathological features between the 2 conditions. Whereas cognitive impairment has been linked to HF through perfusion defects, angiopathy, and inflammation, whether patients with AD present with myocardial dysfunction, and if the 2 conditions bear a common pathogenesis as neglected siblings are unknown. Here, the authors investigated whether amyloid beta (Aβ) protein aggregates are present in the hearts of patients with a primary diagnosis of AD, affecting myocardial function. The authors examined myocardial function in a retrospective cross-sectional study from a cohort of AD patients and age-matched controls. Imaging and proteomics approaches were used to identify and quantify Aβ deposits in AD heart and brain specimens compared with controls. Cell shortening and calcium transients were measured on isolated adult cardiomyocytes. Echocardiographic measurements of myocardial function suggest that patients with AD present with an anticipated diastolic dysfunction. As in the brain, Aβ 40 and Aβ 42 are present in the heart, and their expression is increased in AD. Here, the authors provide the first report of the presence of compromised myocardial function and intramyocardial deposits of Aβ in AD patients. The findings depict a novel biological framework in which AD may be viewed either as a systemic disease or as a metastatic disorder leading to heart, and possibly multiorgan failure. AD and HF are both debilitating and life-threatening conditions, affecting enormous patient populations. Our findings underline a previously dismissed problem of a magnitude that will require new diagnostic approaches and treatments for brain and heart disease, and their combination.

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