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O5‐04‐03: AMYLIN TREATMENT AMELIORATES ABNORMAL PATTERNS OF GENE EXPRESSION IN THE CEREBRAL CORTEX OF AN ALZHEIMER’S DISEASE MOUSE MODEL
Author(s) -
Wang Erming,
Zhu Haihao,
Gower Adam,
Blusztajn Jan Krzysztof,
Kowall Neil W.,
Qiu Wendy
Publication year - 2016
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.2016.06.724
Subject(s) - amylin , transcriptome , microglia , biology , gene expression , amyloid (mycology) , neurodegeneration , neuroscience , genetically modified mouse , gene , transgene , alzheimer's disease , human brain , microbiology and biotechnology , disease , medicine , endocrinology , genetics , immunology , inflammation , botany , islet , insulin
known to contribute to the development of amyloid plaques such as beta amyloid (p<0.001), alpha-synuclein (p<0.001), gelsolin (p<0.01) and GFAP (p<0.0001). Conclusions:We have identified a set of specific proteins that contribute to rapid plaque development in AD and have identified protein networks that are unique to rpAD. Data from this study also provides a new way to examine both the individual proteins as well as protein networks involved in the formation of amyloid plaques, which could provide novel drug targets in the future.