期刊
BIOLOGICAL PSYCHIATRY
卷 83, 期 4, 页码 328-336出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2017.11.031
关键词
Alzheimer's; Aquaporin-4; Astrocytes; Cerebrospinal fluid; CSF; Glymphatic; Interstitial fluid; Perivascular; Sleep
资金
- National Institute on Aging [AG054456, AG008017, AG00817-28]
- National Institute of Neurological Disorders and Stroke [NS089709]
- Paul G. Allen Family Foundation
- GlaxoSmithKline
- Gilead Pharmaceuticals
- Shire
- Genentech
- Neurim Pharmaceuticals
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS089709] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG054456, P30AG008017] Funding Source: NIH RePORTER
Amyloid-beta (A beta) plaques are a key histopathological hallmark of Alzheimer's disease (AD), and soluble A beta species are believed to play an important role in the clinical development of this disease. Emerging biomarker data demonstrate that A beta plaque deposition begins decades before the onset of clinical symptoms, suggesting that understanding the biological determinants of the earliest steps in the development of AD pathology may provide key opportunities for AD treatment and prevention. Although a clinical association between sleep disruption and AD has long been appreciated, emerging clinical studies and insights from the basic neurosciences have shed important new light on how sleep and A beta homeostasis may be connected in the setting of AD. A beta, like many interstitial solutes, is cleared in part through the exchange of brain interstitial fluid and cerebrospinal fluid along a brain-wide network of perivascular pathways recently termed the glymphatic system. Glymphatic function is primarily a feature of the sleeping brain, rather than the waking brain, and is slowed in the aging and posttraumatic brain. These changes may underlie the diurnal fluctuations in interstitial and cerebrospinal fluid A beta levels observed in both the rodent and the human. These and other emerging studies suggest that age-related sleep disruption may be one key factor that renders the aging brain vulnerable to A beta deposition and the development of AD. If this is true, sleep may represent a key modifiable risk factor or therapeutic target in the preclinical phases of AD.
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