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Pregled bibliografske jedinice broj: 38130


Autori: Šimić, Goran; Gnjidić, Maša; Kostović, Ivica
Naslov: Cytoskeletal changes as an alternative view on pathogenesis of Alzheimer's disease
Izvornik: Periodicum biologorum (0031-5362) 100 (1998), 2; 165-173
Vrsta rada: pregledni rad
Ključne riječi: abnormal phospshorylation; dystrophic neurite; neurofibrillary tangle; neuropil thread; tau protein
The main cytoskeletal change and the most characteristic neuropathological lesion in AD is neurofibrillary degeneration. Neurofibrillary degeneration is gradual interneuronal accumulation of paired helical filaments which consist of abnormally phosphorylated microtubule-associated protein tau. Neurofibrillary tangles, neuropil threads and senile plaque dystrophic neurites formed from paired helical filaments develop in only a few types of cortical pyramidal cells and their regional distribution correlates with the degree of dementia. First changes in both 'normal' aging and AD brains are seen in entorhinal cortex. In AD, destructive process then spreads into hippocampal formation and neocortex. While most investigators still believe that beta-amyloid deposition is the central responsible factor in AD, in the last several years many authors have suggested that a more satisfying pathogenetic scheme can be based on the centrality of cytoskeletal abnormality. This concept is supported by the fact that all six identified genes for AD (APP, PS1, PS2, APOE, CO1 and CO2) interact in some way with the cytoskeleton. Cytoskeletal abnormality leads to alterations of the Golgi apparatus with subsequent effects on protein processing and axoplasmic flow. The outcome is a loss of synapses and neurons followed with the disconnection syndrome and dementia. It seems that it takes 20-30 years from the earliest neuronal changes caused by light hyperphosporylation to the development of obvious AD symptoms, because such neurons are only visible in adults over 30. The altered tau protein shown by the antibody AT8 (binds to abnormally phosphorylated Ser-202) is the earliest cytoskeleton change which eventually leads to the formation of paired helical filaments. The roles of microtubule-associated kinases and phosphatases have yet to be fully described, but may lead to identification of therapeutic targets for halting the progression of paired helical filament formation.
Projekt / tema: 0108118
Izvorni jezik: ENG
Current Contents: NE
Citation Index: DA
Kategorija: Ostalo
Znanstvena područja:
Kliničke medicinske znanosti
Tiskani medij: da
Google Scholar: Cytoskeletal changes as an alternative view on pathogenesis of Alzheimer's disease

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