What is it about?
We previously showed that mouse models carrying human Familial Natural Short Sleep genetic mutations can significantly slow the onset and reduce the progression of Alzheimer pathology. Here, we further show evidence supporting that improving sleep quality represents a potential approach to delay the onset and progression of dementia.
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Why is it important?
Age-dependent dementia is one of the largest societal and economic burdens, and the need for strategies to promote healthy aging is becoming increasingly urgent with the trend toward longer life span. Methods to mitigate age-related diseases will significantly impact future human health worldwide. This study supports that improving sleep quality represents a potential approach to delay the onset and progression of dementia.
Perspectives
Although sleep difficulties often accompany neurodegeneration, individuals with the Familial Natural Short Sleep (FNSS) trait rarely suffer from age-related diseases, despite their lifelong short sleep duration, suggesting a potential protective function of FNSS mutations. We took advantage of the mouse models of FNSS and AD to demonstrate that good sleep can help with healthy longevity.
Ying-Hui Fu
University of California San Francisco
Read the Original
This page is a summary of: Mutant β
1
-adrenergic receptor improves REM sleep and ameliorates tau accumulation in a mouse model of tauopathy, Proceedings of the National Academy of Sciences, April 2023, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2221686120.
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