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Alzheimer's disease (AD) pathology disrupts brain-heart signaling, causing cardiac nerve damage and dysfunction. Amyloid-beta (Aβ) oligomers reduce brain-derived neurotrophic factor (BDNF) in heart cells, highlighting a new mechanism for AD-related cardiac issues.

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Area of Science:

  • Neuroscience
  • Cardiology
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) disrupts neurotrophic factors (NTFs), impacting neuronal health and potentially causing cardiovascular issues.
  • Mechanisms linking AD pathology to impaired brain-heart axis, myocardial innervation, and function remain unclear.

Purpose of the Study:

  • To investigate the impact of AD pathology on cardiac physiology and the brain-heart axis.
  • To elucidate the role of amyloid-beta (Aβ) in neurotrophic factor depletion and cardiac neuronal degeneration.

Main Methods:

  • Comprehensive analysis of cardiac physiology, amyloid pathology, NTF depletion, and cardiac neuronal fiber degeneration in AD mouse models, human cardiomyocytes, and human AD heart tissue.
  • Assessment of Aβ oligomer effects on BDNF expression and CREB function in cardiomyocytes.
  • Postmortem analysis of human left ventricular (LV) tissue from AD patients.

Main Results:

  • AD pathology increases myocardial fibrosis, Aβ deposition, and brain-heart axis remodeling, leading to myocardial denervation and impaired cardiac function.
  • Aβ oligomers reduce BDNF expression in human cardiomyocytes by disrupting CREB function.
  • Human AD LV tissue confirmed findings from animal and cell studies.

Conclusions:

  • A previously unrecognized mechanism reveals Aβ dysregulates cardiac neurotrophic signaling, contributing to cardiac degeneration in AD.
  • Findings underscore the significance of cardiac complications in AD management and suggest new therapeutic avenues.
  • Highlights the need to reevaluate clinical approaches to AD therapy by considering cardiac health.