Enriched endogenous n-3 polyunsaturated fatty acids alleviate cognitive and behavioral deficits in a mice model of Alzheimer’s disease

Highlights • Establishment of the APP/fat-1 mice model with enriched endogenous n-3 PUFAs. • High n-3 PUFAs and high ratio of n-3/n-6 PUFAs delay the early symptoms of AD. • Reduced Aβ protein deposition inhibits glial cells activation and neuronal apoptosis.

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Veröffentlicht in:	Neuroscience 2016-10, Vol.333, p.345-355
Hauptverfasser:	Wu, Kefeng, Gao, Xiang, Shi, Baoyan, Chen, Shiyu, Zhou, Xin, Li, Zhidong, Gan, Yuhong, Cui, Liao, Kang, Jingxuan, Li, Wende, Huang, Ren
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer Disease - psychology Alzheimer’s disease Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - metabolism amyloid precursor protein Animals Astrocytes - metabolism Astrocytes - pathology Brain - metabolism Brain - pathology Caenorhabditis elegans Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Cognition - physiology Cognition Disorders - metabolism Cognition Disorders - pathology Diet Disease Models, Animal Fatty Acid Desaturases - genetics Fatty Acid Desaturases - metabolism Fatty Acids, Omega-6 - administration & dosage Humans Maze Learning - physiology Mice, Inbred C57BL Mice, Transgenic Motor Activity - physiology Neurology Neurons - metabolism Neurons - pathology NF-kappa B - metabolism polyunsaturated fatty acids Time Factors
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Beschreibung
Zusammenfassung:	Highlights • Establishment of the APP/fat-1 mice model with enriched endogenous n-3 PUFAs. • High n-3 PUFAs and high ratio of n-3/n-6 PUFAs delay the early symptoms of AD. • Reduced Aβ protein deposition inhibits glial cells activation and neuronal apoptosis.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2016.07.038