Sleep, Aging, and Cellular Health: Aged-Related Changes in Sleep and Protein Homeostasis Converge in Neurodegenerative Diseases

Many neurodegenerative diseases manifest in an overall aged population, the pathology of which is hallmarked by abnormal protein aggregation. It is known that across aging, sleep quality becomes less efficient and protein homeostatic regulatory mechanisms deteriorate. There is a known relationship b...

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Bibliographic Details
Published in:Frontiers in aging neuroscience 2019-06, Vol.11, p.140-140
Main Authors: Hafycz, Jennifer M, Naidoo, Nirinjini N
Format: Article
Language:English
Subjects:
Aging
Autophagy
Cognition & reasoning
Disease
Endoplasmic reticulum
Homeostasis
Hypotheses
neurodegenarative disease
Neurodegeneration
Neurodegenerative diseases
Neuroscience
Neurosciences
Older people
Physiology
Protein folding
Protein interaction
Protein synthesis
proteostasis cell stress and aging
Quality
Signal transduction
Sleep
Sleep and wakefulness
unfolded protein response
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Summary:Many neurodegenerative diseases manifest in an overall aged population, the pathology of which is hallmarked by abnormal protein aggregation. It is known that across aging, sleep quality becomes less efficient and protein homeostatic regulatory mechanisms deteriorate. There is a known relationship between extended wakefulness and poorly consolidated sleep and an increase in cellular stress. In an aged population, when sleep is chronically poor, and proteostatic regulatory mechanisms are less efficient, the cell is inundated with misfolded proteins and suffers a collapse in homeostasis. In this review article, we explore the interplay between aging, sleep quality, and proteostasis and how these processes are implicated in the development and progression of neurodegenerative diseases like Alzheimer's disease (AD). We also present data suggesting that reducing cellular stress and improving proteostasis and sleep quality could serve as potential therapeutic solutions for the prevention or delay in the progression of these diseases.
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2019.00140