Familial natural short sleep mutations reduce Alzheimer pathology in mice.

Autor:	Dong Q; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA., Gentry NW; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA., McMahon T; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA., Yamazaki M; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA., Benitez-Rivera L; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA., Wang T; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA., Gan L; Helen & Robert Appel Alzheimer's Disease Research Institute, Weill Cornell Medicine, New York, NY 10021, USA., Ptáček L; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA.; Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA.; Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA 94143, USA.; Kavli Institute for Fundamental Neuroscience, University of California San Francisco, San Francisco, CA 94143, USA., Fu YH; Department of Neurology, University of California San Francisco, San Francisco, CA 94143, USA.; Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA.; Weill Institute for Neuroscience, University of California San Francisco, San Francisco, CA 94143, USA.; Kavli Institute for Fundamental Neuroscience, University of California San Francisco, San Francisco, CA 94143, USA.
Jazyk:	angličtina
Zdroj:	IScience [iScience] 2022 Mar 15; Vol. 25 (4), pp. 103964. Date of Electronic Publication: 2022 Mar 15 (Print Publication: 2022).
DOI:	10.1016/j.isci.2022.103964
Abstrakt:	Although numerous studies have demonstrated that poor sleep increases the development of AD, direct evidence elucidating the benefits of good sleep on the AD pathogenesis is lacking. Familial Natural Short Sleepers (FNSS) are genetically wired to have lifelong reduction in nightly sleep duration without evident consequence on cognitive demise, implying that they may have better sleep quality. Here we investigated two FNSS mutations, DEC2-P384R and Npsr1-Y206H , on the development of tau and amyloid pathology in AD-like mouse models. We found that the development of tau pathology is attenuated in the hippocampus of tau mice carrying FNSS mutations. We also found that DEC2-P384R;5XFAD and female Npsr1-Y206H;5XFAD mice exhibit significantly less amyloid plaques than control mice at 6 months of age. Together, these results reveal that these two FNSS alleles are strong genetic modifiers of AD pathology and may confer resilience to the progression of tau pathology and amyloid plaque formation in neurodegeneration. Competing Interests: The authors declare no competing interests.
Databáze:	MEDLINE
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