[Does acidosis in brain play a role in Alzheimer's disease?]

Neuropsychiatr. 2009;23(3):187-92.
[Article in German]


Alzheimer's disease is characterized by beta-amyloid plaques, tau pathology, cell death of cholinergic neurons, inflammatory processes and cerebrovascular damage. The reasons for the development of this chronic disease are not known yet. We hypothesize that chronic long lasting mild damage of the cerebrovascular brain capillaries cause hypoperfusion, acidosis and neurodegeneration, and induces a cell death cascade with beta-amyloid dysfunction and tau-pathology and inflammation. Vascular risk factors, such as hyperhomocysteinemia or hypercholesterolemia, may play a role in this process. The accumulation of chronic silent strokes may cause cognitive defects as seen in vascular dementia and Alzheimer's disease. This summary tries to link the different events, which occur in Alzheimer's disease, focusing on the cerebrovascular hypothesis.

Publication types

  • English Abstract

MeSH terms

  • Acidosis / physiopathology*
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / metabolism
  • Blood-Brain Barrier / physiology
  • Brain / physiopathology*
  • Brain Ischemia / physiopathology
  • Cell Death / physiology
  • Cerebral Arteries / physiopathology
  • Cholesterol / metabolism
  • Homocysteine / metabolism
  • Humans
  • Inflammation / physiopathology
  • Lactic Acid / metabolism
  • Neurons / physiology
  • Risk Factors
  • tau Proteins / metabolism


  • Amyloid beta-Peptides
  • tau Proteins
  • Homocysteine
  • Lactic Acid
  • Cholesterol