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P1‐176: Medial prefrontal cortex astrocytes atrophy in Alzheimer's disease
Author(s) -
Kulijewicz-Nawrot Magdalena,
Sykova Eva,
Verkhratsky Alexei,
Rodriguez Arellano Jose J.
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.2010.05.726
Subject(s) - prefrontal cortex , hippocampus , glial fibrillary acidic protein , atrophy , neuroscience , entorhinal cortex , pathology , astrocyte , psychology , biology , medicine , central nervous system , immunohistochemistry , cognition
in B103-wtAPP cells by siRNA targeted to RAGE significantly reduced Ab accumulation, in parallel, inhibited band g-secretase activity and GSK-3b activity. Conclusions: Therefore, we concluded that RAGE-dependent activation of GSK-3b is important mechanism underlying modulation of APP cleavage through regulating b and g secretase activity, which is likely responsible for limiting cerebral Ab accumulation in RAGE-deficiency mAPP mice. Agents that block activation of GSK or inhibite RAGE might provide protection in an Ab milieu of Alzheimer’s disease. Our data support RAGE is a potential therapeutic target to ameliorate cellular dysfunction in Alzheimer’s disease.