FIND ARTICLE

MOLECULAR MECHANISMS OF ALZHEIMER'S DISEASE

Alzheimer's disease is one of the most widespread neurodegenerative disorder. The etiology of this disease is not completely elucidated. Amyloid plaques (extracellular aggregates of amyloid β peptides – Aβ) and neurofibrillary tangles (intracellular deposits of hyperphosphorylated tau protein) are histopa- thological hallmarks of the Alzheimer disease. These morphological changes are present mostly in brain regions involved in cognition, emotion, learning and memory. The critical events in the pathogenesis of Alzheimer's disease are caused by amyloid β peptides.

THE INFLUENCE OF α-SYNUCLEIN ON DOPAMINERGIC SYSTEM FUNCTION

α-Synuclein (ASN) is richly abundant in the central nervous system, particulary in pre- synaptic terminals. Among many functions, ASN plays a crucial role in regulation of dopaminergic system. In physiological conditions, soluble ASN is involved in maintenance of dopamine (DA) homeostasis in the central nervous system. This protein regulates DA level and biosynthesis by inhibition of the tyrosine hydroxylase. It also influences DA storage and release from synaptic ve- sicles as well as DA uptake by its transporter (DAT).

ALPHA-SYNUCLEIN IN PHYSIOLOGY AND PATHOLOGY OF THE BRAIN

Synucleins are a family of small (15–20 kDa), soluble, conserved proteins that are predominan- tly expressed in neurons and include α-, β-, γ-Synuclein and Synoretine. Among the synuclein family exclusively α-Synuclein is the precursor protein for highly hydrophobic 35-amino acid peptide NAC (non-amyloid β component of Alzheimer’s disease plaques). This presynaptic protein associated with synaptic vesicles is also present in cytosol. Under physiological conditions α-Synuclein is natively unfolded.

The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

Editorial address:
Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email: mnowicki@ump.edu.pl

PBK Postępby biologi komórki