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P1‐192: Aβ‐POTENTIATED AND Aβ‐INDEPENDENT AGE RELATED CHANGES IN THE LENS OF THE EYE IN WILD‐TYPE AND ALZHEIMER'S DISEASE MICE
Author(s) -
Moncaster Juliet A.,
Wojnarowicz Mark W.,
Zeng Rebecca,
Minaeva Olga,
Goldstein Lee
Publication year - 2018
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.2018.06.196
Subject(s) - crystallin , genetically modified mouse , lens (geology) , wild type , endocrinology , transgene , disease , medicine , chemistry , biology , neuroscience , microbiology and biotechnology , gene , biochemistry , mutant , paleontology
primary neural cell culture. Results: We found that cognitive deficits in middle-aged PS1V97L trangenic AD mice were mainly caused by the accumulation of nonameric and dodecameric soluble Ab oligomers, which could be produced and duplicated in astrocytes to accelerate neuronal injury by activating b-secretase and apolipoprotein E. Conclusions: Taken together, our results suggest that the astrocytes could augment the production of nonamer and dodecamer leading to neuronal injury and cognitive deficits associated with AD. P1-192 Ab-POTENTIATEDANDAb-INDEPENDENT AGERELATEDCHANGES IN THE LENS OF THE EYE IN WILD-TYPE AND ALZHEIMER’S DISEASE MICE Juliet A. Moncaster, Mark W. Wojnarowicz, Rebecca Zeng, Olga Minaeva, Lee Goldstein, Boston University School of Medicine, Boston, MA, USA; Boston University, Boston, MA, USA. Contact e-mail: jmon@bu.edu