Neuronal Autophagy: Self-eating or Self-cannibalism in Alzheimer's Disease
PBN-AR
Instytucja
Instytut Medycyny Doświadczalnej i Klinicznej im. Mirosława Mossakowskiego Polskiej Akademii Nauk
Informacje podstawowe
Główny język publikacji
en
Czasopismo
Neurochemical Research
ISSN
0364-3190
EISSN
1573-6903
Wydawca
SPRINGER/PLENUM PUBLISHERS
DOI
URL
Rok publikacji
2013
Numer zeszytu
9
Strony od-do
1769-1773
Numer tomu
38
Identyfikator DOI
Liczba arkuszy
0,68
Słowa kluczowe
en
Alzheimer's disease
Autophagy
Amyloid precursor protein
beta-Amyloid peptide
tau-Protein
Neuronal death
Open access
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Język
en
Treść
Autophagy is a major intracellular degeneration pathway involved in the elimination and recycling of damaged organelles and long-lived proteins by lysosomes. Many of the pathological factors, which trigger neurodegenerative diseases, can perturb the autophagy activity, which is associated with misfolded protein aggregates accumulation in these disorders. Alzheimer's disease, the first neurodegenerative disorder between dementias, is characterized by two aggregating proteins, beta-amyloid peptide (plaques) and tau-protein (tangles). In Alzheimer's disease autophagosomes dynamically form along neurites within neuronal cells and in synapses but effective clearance of these structures needs retrograde transportation towards the neuronal soma where there is a major concentration of lysosomes. Maturation of autophago-lysosomes and their retrograde trafficking are perturbed in Alzheimer's disease, which causes a massive concentration of autophagy elements along degenerating neurites. Transportation system is disturbed along defected microtubules in Alzheimer's disease brains. tau-protein has been found to control the stability of microtubules, however, phosphorylation of tau-protein or an increase in the total level of tau-protein can cause dysfunction of neuronal cells microtubules. Current evidence has shown that autophagy is developing in Alzheimer's disease brains because of ineffective degradation of autophagosomes, which hold amyloid precursor protein-rich organelles and secretases important for beta-amyloid peptides generation from amyloid precursor. The combination of raised autophagy induction and abnormal clearance of beta-amyloid peptide-generating autophagic vacuoles creates circumstances helpful for beta-amyloid peptide aggregation and accumulation in Alzheimer's disease. However, the key role of autophagy in Alzheimer's disease development is still under consideration today. One point of view suggests that abnormal autophagy induction causes a concentration of autophagic vacuoles rich in amyloid precursor protein, beta-amyloid peptide and the elements crucial for its formation, whereas other hypothesis points to marred autophagic clearance or even decrease in autophagic effectiveness playing a role in maturation of Alzheimer's disease. In this review we present the recent evidence linking autophagy to Alzheimer's disease and the role of autophagic regulation in the development of full-blown Alzheimer's disease.
Cechy publikacji
REVIEW_ARTICLE
Inne
System-identifier
592358
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