The Emerging Relationship Between Interstitial Fluid-Cerebrospinal Fluid Exchange, Amyloid-β, and Sleep

被引:121
作者
Boespflug, Erin L. [1 ,2 ]
Iliff, Jeffrey J. [3 ,4 ]
机构
[1] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97201 USA
[2] Oregon Hlth & Sci Univ, Adv Imaging Res Ctr, Portland, OR 97201 USA
[3] Oregon Hlth & Sci Univ, Dept Anesthesiol & Perioperat Med, 3181 SW Sam Jackson Pk Rd,Mail Code L458, Portland, OR 97239 USA
[4] Oregon Hlth & Sci Univ, Knight Cardiovasc Inst, Portland, OR 97201 USA
关键词
Alzheimer's; Aquaporin-4; Astrocytes; Cerebrospinal fluid; CSF; Glymphatic; Interstitial fluid; Perivascular; Sleep; CENTRAL-NERVOUS-SYSTEM; VIRCHOW-ROBIN SPACES; MILD COGNITIVE IMPAIRMENT; BLOOD-BRAIN-BARRIER; NORMAL-PRESSURE HYDROCEPHALUS; ALZHEIMERS-DISEASE; GLYMPHATIC PATHWAY; RAT-BRAIN; AQUAPORIN EXPRESSION; PERIVASCULAR SPACES;
D O I
10.1016/j.biopsych.2017.11.031
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:328 / 336
页数:9
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