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 ?
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]