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P2‐269: Induction of cerebral amyloidosis and memory impairments by blood transfusion in mice models of Alzheimer's disease
Author(s) -
Morales Rodrigo,
DuranAniotz Claudia,
Urayama Akihiko,
Estrada Lisbell D,
MoralesScheihing Diego,
Soto Claudio
Publication year - 2011
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.2011.05.1148
Subject(s) - pathogenesis , hippocampus , genetically modified mouse , medicine , amyloidosis , pathology , pathological , immunohistochemistry , cerebral cortex , inflammation , memory impairment , disease , transgene , biology , gene , cognition , biochemistry , psychiatry
transcription of genes involved in protein quality control and degradation pathways as well as fly homologue of As degrading enzymes. In addition, genes known to be induced by stresses were up regulated by Sin3A knockdown, and overexpression of these genes suppressed As42 toxicity without altering As accumulation.We further demonstrated that these genes were up regulated in human neuroblastoma SH-SY5Y cells treated with HDAC inhibitors.Conclusions:Our results indicate that multiple mechanisms underlie protective effects of inhibition of Sin3A/HDACs activity against As42induced toxicity.