A β-amiloid és a mitochondrialis diszfunkció szerepe az Alzheimer-kór patogenezisében

Translated title of the contribution: The role of β-amyloid and mitochondrial dysfunction in the pathogenesis of Alzheimer's disease

Research output: Contribution to journalReview article

2 Citations (Scopus)

Abstract

Alzheimer's disease is the most common form of dementia in mid- and late life. The 7-10% of the population over 65 and the 50-60% of the population over 85 are affected by this disease. On the contrary of its prevalence the pathogenesis of the disease is not well defined and there is no effective neuroprotective therapeutic agent. Three predominant neuropathological features of the Alzheimer's disease brain are intracellular neurofibrillary tangles consisting mainly of the hyperphosphorylated protein T; the extracellular amyloid deposits (neuritic plaques) consisting of amyloid β peptide; and the extensive neuronal cell loss in the hippocampus and in portions of the cerebral cortex. The possible reason of the extensive neuronal cell loss can be the mitochondrial dysfunction observed in Alzheimer's disease. Beyond the unclarified pathogenesis the causality of these characteristic neuropathologic phenomena are still unknown. In this study we would like to deal with two actual hypotheses, with the amyloid cascade and with the mitochondrial cascade hypotheses. We try to give an overview of these two hypotheses and to depict their interrelationship.

Translated title of the contributionThe role of β-amyloid and mitochondrial dysfunction in the pathogenesis of Alzheimer's disease
Original languageHungarian
Pages (from-to)222-228
Number of pages7
JournalIdeggyogyaszati szemle
Volume68
Issue number7-8
DOIs
Publication statusPublished - Jul 30 2015

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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