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Ahmadian N, Hejazi S, Mahmoudi J, et al. Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation. Basic Clin Neurosci. 2018;9(5):307-316doi: 10.32598/bcn.9.5.307.
Ahmadian, N., Hejazi, S., Mahmoudi, J., & Talebi, M. (2018). Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation. Basic and clinical neuroscience, 9(5), 307-316. https://doi.org/10.32598/bcn.9.5.307
Ahmadian, Nahid, et al. "Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation." Basic and clinical neuroscience vol. 9,5 (2018): 307-316. doi: https://doi.org/10.32598/bcn.9.5.307
Ahmadian N, Hejazi S, Mahmoudi J, Talebi M. Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation. Basic Clin Neurosci. 2018 Sep-Oct;9(5):307-316. doi: 10.32598/bcn.9.5.307. Epub 2018 Sep 01. PMID: 30719245; PMCID: PMC6360494.
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Basic Clin Neurosci. 2018 Sep-Oct;9(5):307-316. doi: 10.32598/bcn.9.5.307. Epub 2018 Sep 01.

Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation.

Basic and clinical neuroscience

Nahid Ahmadian, Sajjad Hejazi, Javad Mahmoudi, Mahnaz Talebi

Affiliations

  1. Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
  2. Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
  3. Department of Anatomy, Faculty of Veterinary Medicine, Tabriz Branch, Islamic Azad University, Tabriz, Iran.

PMID: 30719245 PMCID: PMC6360494 DOI: 10.32598/bcn.9.5.307

Abstract

Sleep deprivation is a common complaint in modern societies. Insufficient sleep has increased the risk of catching neurodegenerative diseases such as Alzheimer's. Several studies have indicated that restricted sleep increases the level of deposition of β-amyloid and formation of neurofibrillary tangles, the major brain microstructural hallmarks for Alzheimer disease. The mechanisms by which sleep deprivation affects the pathology of Alzheimer disease has not yet been fully and definitively identified. However, risk factors like apolipoprotein E risk alleles, kinases and phosphatases dysregulation, reactive oxygen species, endoplasmic reticulum damages, glymphatic system dysfunctions and orexinergic system inefficacy have been identified as the most important factors which mediates between the two conditions. In this review, these factors are briefly discussed.

Keywords: Alzheimer’s disease; Amyloid beta-peptides; Amyloid beta-protein precursor; Neurofilament proteins; Sleep disorder; Tau proteins

Conflict of interest statement

Conflict of interest The authors declare no conflict of interest.

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