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Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation

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 tang...

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Autores principales: Ahmadian, Nahid, Hejazi, Sajjad, Mahmoudi, Javad, Talebi, Mahnaz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Iranian Neuroscience Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6360494/
https://www.ncbi.nlm.nih.gov/pubmed/30719245
http://dx.doi.org/10.32598/bcn.9.5.307
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author Ahmadian, Nahid
Hejazi, Sajjad
Mahmoudi, Javad
Talebi, Mahnaz
author_facet Ahmadian, Nahid
Hejazi, Sajjad
Mahmoudi, Javad
Talebi, Mahnaz
author_sort Ahmadian, Nahid
collection PubMed
description 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.
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spelling pubmed-63604942019-02-04 Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation Ahmadian, Nahid Hejazi, Sajjad Mahmoudi, Javad Talebi, Mahnaz Basic Clin Neurosci Review Paper 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. Iranian Neuroscience Society 2018 2018-09-01 /pmc/articles/PMC6360494/ /pubmed/30719245 http://dx.doi.org/10.32598/bcn.9.5.307 Text en Copyright© 2018 Iranian Neuroscience Society http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Paper
Ahmadian, Nahid
Hejazi, Sajjad
Mahmoudi, Javad
Talebi, Mahnaz
Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation
title Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation
title_full Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation
title_fullStr Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation
title_full_unstemmed Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation
title_short Tau Pathology of Alzheimer Disease: Possible Role of Sleep Deprivation
title_sort tau pathology of alzheimer disease: possible role of sleep deprivation
topic Review Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6360494/
https://www.ncbi.nlm.nih.gov/pubmed/30719245
http://dx.doi.org/10.32598/bcn.9.5.307
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