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P3‐381: Increasing glutathione export by astrocytes: A novel therapeutic principle for the treatment of Alzheimer's disease?
Author(s) -
Muench Gerald,
Steele Megan L.
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.2010.05.1923
Subject(s) - glutathione , oxidative stress , proinflammatory cytokine , reactive oxygen species , chemistry , neurodegeneration , biochemistry , microglia , microbiology and biotechnology , inflammation , biology , immunology , enzyme , medicine , disease
age, and therefore were considered unlikely to be due to the accumulation of oligomeric Abeta. These deficits were not affected by drug treatment. Transcriptional profiles of animals treated with drug compared to vehicle showed evidence of regulation of pathways related to synaptic plasticity and remodeling of the dendritic cytoskeleton, consistent with stabilization of vulnerable spine structure. Conclusions: This data supports the hypothesis that PDE9 inhibition can stabilize vulnerable synapses early in the Alzheimer’s disease process.