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

Dec 28, 2017Biological psychiatry

How Fluid Exchange Between Brain Spaces, Amyloid-Beta, and Sleep May Be Connected

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Abstract

Aβ plaque deposition may begin decades before clinical symptoms of Alzheimer's disease appear.

Soluble Aβ species are believed to play a significant role in the development of Alzheimer's disease.
Sleep disruption has a recognized clinical association with Alzheimer's disease.
Glymphatic function, responsible for clearing Aβ, is primarily active during sleep.
Aging and posttraumatic changes may slow glymphatic function, impacting Aβ clearance.
Diurnal fluctuations in Aβ levels have been observed in both rodent and human studies.
Age-related sleep disruption could increase vulnerability to Aβ deposition and Alzheimer's disease.

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Amyloid-β (Aβ) plaques are a key histopathological hallmark of Alzheimer's disease (AD), and soluble Aβ species are believed to play an important role in the clinical development of this disease. Emerging biomarker data demonstrate that Aβ 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 Aβ homeostasis may be connected in the setting of AD. Aβ, 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 Aβ 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 Aβ 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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The Emerging Relationship Between Interstitial Fluid–Cerebrospinal Fluid Exchange, Amyloid-β, and Sleep

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