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P1‐131: MODEL‐AD: LATE‐ONSET ALZHEIMER'S DISEASE MODELS
Author(s) -
Lamb Bruce T.,
Oblak Adrian L.,
Williams Harriet M.,
Baglietto-Vargas David,
Wood Marcelo A.,
Mortazavi Ali,
Green Kim N.,
Carter Gregory W.,
Sukoff Rizzo Stacey J.,
Territo Paul,
Sasner Michael,
Macgregor Grant R.,
Tenner Andrea,
LaFerla Frank,
Howell Gareth
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.2018.06.134
Subject(s) - trem2 , neurodegeneration , disease , phenotype , alzheimer's disease , computational biology , medicine , bioinformatics , genetic model , animal model , dementia , allele , biology , neuroscience , genetics , gene , pathology , immunology , inflammation , microglia
function (rotarod and pole tests), memory (8-arm radial arm maze), and anxiety (open field). In addition, brain, spinal cord, and muscle were evaluated by histology and biochemistry. Results:Our results indicate mild motor deficits on the grip strength test from the NEFH/A315Tmice. Rotarod and 8-arm radial maze showed no significant deficiencies comparing the hTDP-43 and A315T expressing mice. We do see an accumulation of phosphorylated TDP-43 positive neurons and some change in muscle organization present in the A315T mouse, though little motor deficit is evident in the mice at 10-months of age. Conclusions:Although we observe just moderate changes in motor function, this model may provide insight into understanding the early pathological markers associated with the pathogenesis of ALS.