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The Sleep Side of Aging and Alzheimer's Disease

期刊

SLEEP MEDICINE
卷 77, 期 -, 页码 209-225

出版社

ELSEVIER
DOI: 10.1016/j.sleep.2020.05.029

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资金

  1. BROAD Institute at Harvard-MIT (Boston, MA, USA) [2016P000351]
  2. Defence Advanced Research Projects Agency (DARPA) Emiliano Santarnecchi [HR001117S0030]
  3. Beth Israel Deaconess Medical Center (BIDMC)
  4. NIH [R01 AG060981-01]
  5. [R01 MH117063-01]
  6. [P01 AG031720]

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As individuals age, their sleep patterns change, affecting cognitive abilities and quality of life. These changes are associated with alterations in brain structure and function, with sleep abnormalities potentially accelerating the pathophysiology of Alzheimer's Disease.
As we age, sleep patterns undergo significant modifications in micro and macrostructure, worsening cognition and quality of life. These are associated with remarkable brain changes, like deterioration in synaptic plasticity, gray and white matter, and significant modifications in hormone levels. Sleep alterations are also a core component of mild cognitive impairment (MCI) and Alzheimer's Disease (AD). AD night time is characterized by a gradual decrease in slow-wave activity and a substantial reduction of REM sleep. Sleep abnormalities can accelerate AD pathophysiology, promoting the accumulation of amyloid-beta (A beta) and phosphorylated tau. Thus, interventions that target sleep disturbances in elderly people and MCI patients have been suggested as a possible strategy to prevent or decelerate conversion to dementia. Although cognitive-behavioral therapy and pharmacological medications are still first-line treatments, despite being scarcely effective, new interventions have been proposed, such as sensory stimulation and Noninvasive Brain Stimulation (NiBS). The present review outlines the current state of the art of the relationship between sleep modifications in healthy aging and the neurobiological mechanisms underlying age-related changes. Furthermore, we provide a critical analysis showing how sleep abnormalities influence the prognosis of AD pathology by intensifying A beta and tau protein accumulation. We discuss potential therapeutic strategies to target sleep disruptions and conclude that there is an urgent need for testing new therapeutic sleep interventions. (C) 2020 Elsevier B.V. All rights reserved.

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