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[P4–363]: THE MIND DIET IS ASSOCIATED WITH REDUCED INCIDENCE OF 12‐YEAR COGNITIVE IMPAIRMENT IN AN AUSTRALIAN SETTING
Author(s) -
Hosking Diane E.,
Eramudugolla Ranmalee,
Anstey Kaarin J.
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.2017.06.2234
Subject(s) - cognition , cognitive decline , logistic regression , medicine , gerontology , population , odds , disease , odds ratio , stroke (engine) , demography , psychology , clinical psychology , psychiatry , dementia , environmental health , mechanical engineering , sociology , engineering
impact of common nutrients on brain function in a controlled setting. Most of the focus has been on lipids and polyphenols, but amino acids can also impact brain health. Branched-chain amino acids (BCAA) are commonly used as dietary supplements to increase muscular mass. BCAA alters the ratios of amino acids transported into the brain, including precursors of monoamines, thereby impacting brain function. High levels of circulating BCAAare associated with metabolic risk factors of AD, but direct link with AD remains speculative.We thus investigated the impact of dietaryBCAA on object recognition and neuropathological hallmarks of AD in an animal model.Methods:We have been using the 3xTg-AD model of Ab/Tau neuropathology to determine the effects of nutraceutical interventions on cognitive performance and AD-like pathology. 3xTg-AD mice were fed either a control (CD) or a high-fat diet (HFD) from 6 to 16 months and then to high (+50%), normal (+0%) or low (-50%) BCAA intake from 16 to 18 months of age. Results:Two-third of mice fed HFD supplemented in BCAAdid not survive the 2-month treatment, possibly due to hepatic and muscle toxicity. In addition to increasing plasma BCAA, dietary BCAA treatment led to higher threonine, tryptophan and serotonin levels in the brain. Combining BCAAwith high BCAA intake aggravated cortical tau pathology (insoluble tau pSer202/Thr205: +151%; soluble tau pSer202/Thr205: +271%; pThr231: +680%; pThr181: +93%), without affecting amyloid levels. Finally, mice on the low BCAA diets performed better at the novel object recognition task than mice on other diets. Conclusions: These results indicate that BCAA, in synergy with HFD, induce systemic toxicity and worsen AD-like pathology in 3xTg-AD mice, whereas reducing BCAA intake improves memory performance. These preclinical data underscore a potential risk of combining high-fat and high-BCAA consumption and potential benefits from BCAA restriction in AD.