作者: Julie Lalande , Hélène Halley , Stéphane Balayssac , Véronique Gilard , Sébastien Déjean
DOI: 10.3233/JAD-130023
关键词: Genetically modified mouse 、 Taurine 、 Biochemistry 、 Hippocampal formation 、 Rhinal cortex 、 Internal medicine 、 Hippocampus 、 Endocrinology 、 Cognitive decline 、 Creatine 、 Cerebellum 、 Biology
摘要: In the quest for biomarkers of onset and progression Alzheimer's disease, a 1H NMR-based metabolomic study was performed on simple single-transgenic Tg2576 mouse model. These mice develop slow cognitive decline starting by 6 months express amyloid plaques from 10 age. The metabolic profiles extracts five brain regions (frontal cortex, rhinal hippocampus, midbrain, cerebellum) male were compared to those controls, at 1, 3, 11 most obvious differences due regions. Age also discriminating parameter. Metabolic perturbations already detected in hippocampus cortex transgenic as early 1 month age with decreased concentrations glutamate (Glu) N-acetylaspartate (NAA) wild-type animals. changes more numerous 3 month-old involved Glu, NAA, myo-inositol, creatine, phosphocholine, γ-aminobutyric acid (only hippocampus) whose decreased. A disruption characterized an increase hippocampal taurine mice. At this time point, chemical profile cerebellum slightly affected. months, all analyzed (except frontal cortex) metabolically altered, mainly marked formation neuroprotective metabolites creatine taurine. Our findings demonstrate that modifications occur long before behavioral impairment.