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P3‐436: Aminoff suffering syndrome and decubitus ulcers in advanced dementia
Author(s) -
Aminoff Bechor Z.
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.1978
Subject(s) - dementia , medicine , cronbach's alpha , scale (ratio) , vascular dementia , gerontology , psychometrics , clinical psychology , disease , physics , quantum mechanics
from both the PD and AD programs reduced specifically membrane-associated alpha-synuclein and TAU, repectively. This activity may be therapeutically very relevant since protein-aggregation is not only facilitated by membrane structures but also disturbs its integrity and so setting-off a cascade of events (such as Golgi fragmentation as is observed in neurons early in disease) leading to neuronal degeneration. Mode-of-action studies in yeast and neuronal cell models were performed to reveal the pathway and to identify their corresponding molecular binding partners (targets) whose modulation by the compounds is responsible for the neuroprotective activity. Chemo-genetic and synthetic toxicity screening revealed that both molecules intervene in the endosome-to-lysosome sorting pathway by increasing vesicular-driven transport to lysosomes. Conclusions: The data suggests that ReS9-S and ReS19-T selectively and specifically facilitate lysosome-dependent clearance of pathological species of alpha-synuclein and TAU.