Premium
[P2–122]: CDK5RAP2 GENE AND TAU PATHOPHYSIOLOGY IN LATE‐ONSET SPORADIC ALZHEIMER's DISEASE
Author(s) -
Miron Justin,
Picard Cynthia,
Frappier Josée,
Dea Doris,
Théroux Louise,
Nilsson Nathalie I.V.,
Poirier Judes
Publication year - 2017
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.2017.06.772
Subject(s) - biology , genotyping , single nucleotide polymorphism , temporal cortex , microbiology and biotechnology , population , pathology , human brain , genome wide association study , alzheimer's disease , cerebellum , gene , genetics , genotype , medicine , neuroscience , disease , environmental health
that results in increased amyloid beta levels. Results:We will report our results and discuss how they relate to the relationship between these mutations and both chemokine and amyloid beta levels in mammalian cell lines. Conclusions: This work will allow us to examine the role that amyloid beta plays in the activation of pro-inflammatory responses by the chemokine receptors CCBP2 and CCLR2 and their respective mutants. This work could lead to a means of regulating amyloid beta production and expression which could lead to novel therapeutic solutions.