Open AccessDietary intake of branched‐chain amino acids in a mouse model of Alzheimer's disease: Effects on survival, behavior, and neuropathology
Author(s) -
Tournissac Marine,
Vandal Milene,
Tremblay Cyntia,
Bourassa Philippe,
Vancassel Sylvie,
Emond Vincent,
Gangloff Anne,
Calon Frederic
Publication year - 2018
Publication title -
alzheimer's and dementia: translational research and clinical interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.49
H-Index - 30
ISSN - 2352-8737
DOI - 10.1016/j.trci.2018.10.005
Subject(s) - neuropathology , medicine , endocrinology , amino acid , branched chain amino acid , animal model , neurotransmitter , disease , biology , biochemistry , central nervous system , leucine
High levels of plasmatic branched‐chain amino acids (BCAA), commonly used as dietary supplements, are linked to metabolic risk factors for Alzheimer's disease (AD). BCAA directly influence amino acid transport to the brain and, therefore, neurotransmitter levels. We thus investigated the impact of BCAA on AD neuropathology in a mouse model. Methods 3xTg‐AD mice were fed either a control diet or a high‐fat diet from 6 to 18 months of age. For the last 2 months, dietary BCAA content was adjusted to high (+50%), normal (+0%), or low (−50%). Results Mice fed a BCAA‐supplemented high‐fat diet displayed higher tau neuropathology and only four out of 13 survived. Mice on the low‐BCAA diet showed higher threonine and tryptophan cortical levels while performing better on the novel object recognition task. Discussion These preclinical data underscore a potential risk of combining high‐fat and high BCAA consumption, and possible benefits from BCAA restriction in AD.