Author/Editor     Currais, Antonio; Malik, Bilal; Hortobagyi, Tibor; Soriano, Salvador
Title     The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease
Translated title     Nevronski celični ciklus kot patogenetski dejavnik pri Alzheimerjevi bolezni
Type     članek
Source     Zdrav Vestn
Vol. and No.     Letnik 77, št. Suppl 2
Publication year     2008
Volume     str. II-13-20
Language     eng
Abstract     Differentiated neurons display specific biochemical, physiological and morphological properties that apparently prevent them from further cell division. Nevertheless, expression of cell cycle modulators persists after neuronal differentiation and is upregulated under stress conditions, such as trophic factor deprivation, oxidative stress and the presence of DNA damaging agents. This apparent reactivation of the cell cycle has been postulated as a sine qua non for neuronal death in response to those stress conditions, particularly in Alzheimer's disease. However, the physiological and pathogenic implications of a putative neuronal cell cycle are far from clear. Here, we discuss the notion of the neuronal cell cycle as a mediator of cell death in Alzheimer's disease.
Summary     Specifične biokemične, fiziološke in morfološke lastnosti diferenciranih nevronov preprečujejo njihove nadaljnje celične delitve. Vendar pa nevroni ohranijo izražanje modulatorjev celičnega ciklusa, ki se dodatno poveča ob prisotnosti škodljivih dejavnikov, kot so odtegnitev trofičnih faktorjev, oksidativni stres ali prisotnost snovi, ki poškodujejo DNK. Čeprav vloga reaktivacije celičnega ciklusa in njene fiziološke ter patološke posledice ostajajo v veliki meri nepojasnjene, je reaktivacija celičnega ciklusa verjetno nujen dogodek na poti do smrti nevrona pod vplivom škodljivih dejavnikov, kar še posebno drži za Alzheimerjevo bolezen. Namen podanega pregleda je osvetliti vlogo celičnega ciklusa kot posrednika celične smrti nevronov pri Alzheimerjevi bolezni.
Descriptors     ALZHEIMER'S DISEASE
CELL CYCLE
CELL CYCLE PROTEINS
NEURONS
APOPTOSIS
CYCLINS
OXIDATIVE STRESS
DNA DAMAGE