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Alzheimer’s disease (AD) is the most frequent progressive neurodegenerative   disorder in elderly associated with irreversible cognitive impairment and   dementia. The vast majority of AD patients are sporadic (SAD) in which the   disease develops after age of 65. Despite of century of research, we lack   understanding of the SAD etiology and pathogenesis. Several hypotheses try to   explain the main causes of brain degeneration in SAD, one of them assuming   that genomic instability and the reentry of certain neurons into the   incomplete cell cycle may be the pathogenic basis of the disease. Although   the brain is the most affected organ in AD, numerous studies showed   structural and functional alterations in peripheral tissues, suggesting that   AD is a generalized systemic disorder. Diverse changes in peripheral cells   from AD patients are described in literature including cell cycle aberration   and chromosome instability, alterations in cell viability, proliferation and   apoptosis, oxidative metabolism, amyloid precursor protein and amyloid β   protein metabolism, and other cellular processes. The aim of this paper was   to summarize and review the results of our investigations and the growing   literature data concerning the multiple chromosomal alterations in peripheral   cells of AD patients and to consider their possible role in the disease   pathogenesis as well as the importance of such investigations. [Projekat   Ministarstva nauke Republike Srbije, br. 173034

Cytogenetic alterations in peripheral cells of Alzheimer’s disease patients