A krónikus agyi hipoperfúzió szerepe az Alzheimer-kór kialakulásában--tények es hipotézisek.

Translated title of the contribution: The role of chronic brain hypoperfusion in the pathogenesis of Alzheimer's disease--facts and hypotheses

Dénes Zádori, Zsolt Datki, Botond Penke

Research output: Contribution to journalReview article

12 Citations (Scopus)

Abstract

In Alzheimer's disease, which belongs to the neurodegenerative disorders, the ethiopathogenetic role of several risk factors has been proved. A considerable number of them are mainly known as cardiovascular risk factors and can precipitate chronic brain hypoperfusion. Using functional imaging techniques, this hypoperfusion and the resulting hypometabolism become detectable in the watershed areas of the brain as early as in the stage of mild cognitive impairment. Hypoperfusion leads to the degeneration of capillaries in this area causing the deterioration of diffusion. The further reduction of nutrient and oxygen support of neurons is capable to initiate a neurodegenerative process which spreads along the glutaminergic system arising from the neurons of the association cortices. The neuropathological lesions of this neuronal system, such as the neurofibrillary tangles and the beta-amyloid plaques, are known to be the characteristic markers of Alzheimer's disease. In our review we present the development of hypoperfusion and its consequences in the watershed areas of the brain and describe the neurodegenerative process of the neuronal system arising from the neurons of the association cortices in the early stage of Alzheimer's disease. Considering the previous hypotheses and the neuropathological lesions of Alzheimer's disease we give a new consensus model to characterize the pathomechanism of the disorder.

Original languageHungarian
Pages (from-to)428-437
Number of pages10
JournalIdeggyógyászati szemle
Volume60
Issue number11-12
Publication statusPublished - Nov 30 2007

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ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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