Cerebrovascular damage as a cause for Alzheimer's disease

Curr Neurovasc Res. 2005 Oct;2(4):341-7. doi: 10.2174/156720205774322610.

Abstract

Alzheimer's disease is a progressive brain disorder that gradually destroys a patient's memory function and ability to carry out daily activities. According to the prevailing amyloid cascade hypothesis, Alzheimer's disease is initiated by amyloid beta-peptide accumulation leading to neuronal toxicity. The neurofibrillary tangle deriving from hyperphosphorylated tau and synapse loss are also key features for Alzheimer's disease. Recent studies revealed a significant co-morbidity of Alzheimer's disease and cerebrovascular disease suggesting that cerebrovascular dysregulation is an important feature of Alzheimer's disease. This mini-review will discuss the hypothesis that a dysfunction of the vascular system may result in damage of the neurovascular unit, initiating a cascade of events. An overlap with other forms of cognitive impairment, such as mild cognitive impairment, or vascular dementia will be discussed.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / etiology*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Brain / blood supply
  • Brain / metabolism
  • Brain / physiopathology
  • Cerebral Arteries / metabolism
  • Cerebral Arteries / pathology
  • Cerebral Arteries / physiopathology
  • Cerebrovascular Disorders / complications*
  • Cerebrovascular Disorders / metabolism
  • Cerebrovascular Disorders / physiopathology*
  • Cholinergic Fibers / metabolism
  • Cholinergic Fibers / pathology
  • Cognition Disorders / metabolism
  • Cognition Disorders / pathology
  • Cognition Disorders / physiopathology
  • Dementia, Vascular / metabolism
  • Dementia, Vascular / pathology
  • Dementia, Vascular / physiopathology
  • Humans
  • Models, Neurological

Substances

  • Amyloid beta-Peptides