Association between Sleep, Alzheimer’s, and Parkinson’s Disease
1
Advanced Interdisciplinary Research Division, Frontier Research Institute for Interdisciplinary Sciences, Tohoku University, Sendai 980-8578, Japan
2
Super-Network Brain Physiology, Graduate School of Life Sciences, Tohoku University, Sendai 980-8577, Japan
3
Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan
*
Author to whom correspondence should be addressed.
Biology 2021, 10(11), 1127; https://doi.org/10.3390/biology10111127
Submission received: 28 September 2021
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Revised: 28 October 2021
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Accepted: 30 October 2021
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Published: 3 November 2021
(This article belongs to the Special Issue Protein Folding, Aggregation, and Cell Death)
Simple Summary
Protein misfolding and aggregation in the brain are associated with various neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Sleep impairments are frequently observed in AD and PD patients not only as accompanying symptoms, but also as a prodrome that precedes the onset of these diseases. This suggests the potential of sleep impairments as a biomarker for the early diagnosis of, or as a target of, the treatment of these neurodegenerative diseases.
Abstract
The majority of neurodegenerative diseases are pathologically associated with protein misfolding and aggregation. Alzheimer’s disease (AD) is a type of dementia that slowly affects memory and cognitive function, and is characterized by the aggregation of the β-amyloid protein and tau neurofibrillary tangles in the brain. Parkinson’s disease (PD) is a movement disorder typically resulting in rigidity and tremor, which is pathologically linked to the aggregation of α-synuclein, particularly in dopaminergic neurons in the midbrain. Sleep disorders commonly occur in AD and PD patients, and it can precede the onset of these diseases. For example, cognitively normal older individuals who have highly fragmented sleep had a 1.5-fold increased risk of subsequently developing AD. This suggests that sleep abnormalities may be a potential biomarker of these diseases. In this review, we describe the alterations of sleep in AD and PD, and discuss their potential in the early diagnosis of these diseases. We further discuss whether sleep disturbance could be a target for the treatment of these diseases.
