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P1‐016: Sustained Effect of Cold Exposure on TAU Phosphorylation: Relevance for Alzheimer’s Disease
Author(s) -
Tournissac Marine,
Vandal Milene,
Tremblay Cyntia,
Planel Emmanuel,
Calon Frederic
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.2016.06.763
Subject(s) - phosphorylation , chemistry , medicine , endocrinology , period (music) , biochemistry , physics , acoustics
angiopathy (CAA), which compromises cerebrovasculature and induces neurotoxicity, resulting in cognitive impairment. Physical exercise is one of the most robust non-pharmacological stimulants of brain function, capable of circumventing cognitive deficits observed in AD. The present work examined the extent to which the brain is capable of adapting to or reversing Ab-induced changes under running and sedentary conditions. We hypothesized that physical exercise supports memory function bymaintaining normal vasculature and neurogenesis while stabilizing plaque and CAA pathology in TgCRND8 mouse model of amyloidosis.Methods: Mice at a disease state with established plaque pathology and cognitive deficits were used in this study. Non-transgenic littermates and standard housing conditions were used as controls. After 1, 2, or 3 months of running, animals were assessed for spatial memory with the Y-maze task. Brains were collected 24 hours later for analysis. Neurogenesis and plaque pathology were quantified after 1 and 2 months of running whereas hippocampal vasculature and CAAwere evaluated after 3 months of running. Results: Our results indicate that in TgCRND8 mice running for one month, spatial memory was restored to non-transgenic levels, while neurogenesis and plaque burden were not significantly affected by exercise. In TgCRND8 mice running for two months, spatial memory and neuronal maturation were improved and plaque load was attenuated. Lastly, in transgenic mice running for 3 months, hippocampal vascular morphology was normalized, CAA was reduced, and spatial memory was preserved. Conclusions: This work suggests that physical exercise is an attractive treatment strategy capable of addressing AD pathologies. It provides evidence that physical activity should be included as part of the multimodal regimen along with pharmacologics and cognitive stimulation to alleviate AD pathologies.