Liens entre sommeil et maladie d’Alzheimer : impact du sexe féminin
Abstract
The leading cause of dementia is Alzheimer’s disease (AD). AD disproportionately affects women, a difference that cannot be explained solely by longer life expectancy but rather reflects sex-dependent biological mechanisms. In recent years, sleep disturbances have emerged as a potential modifiable risk factor for AD, as they appear early in the disease course – often preceding cognitive symptoms – and are associated with the accumulation of amyloid and tau pathology. This narrative review synthesizes evidence from human studies examining the influence of biological sex on the relationship between sleep and AD, with a particular focus on obstructive sleep apnea, insomnia, alterations in sleep architecture and microstructure, and circadian rhythm disturbances. A growing body of literature suggests that women may be more vulnerable to the neurocognitive consequences of sleep disturbances, particularly around the menopausal transition, a period characterized by profound hormonal changes that may interact with neurodegenerative processes. Despite this emerging evidence, studies explicitly integrating biological sex, hormonal status, and their interactions with sleep remain very scarce, with some findings showing heterogeneity. This review highlights the need for future research incorporating such data, using stratified and longitudinal designs, to improve our understanding of the mechanisms linking sleep and AD, and to optimize personalized prevention and management strategies for AD.
Related
- Utilisation du lecanemab au stade précoce de la maladie d’Alzheimer au Canada.
- Sentiment de reconnaissance vis-à-vis d’autrui et maladie d’Alzheimer : à propos d’un cas
- Instrumentalisation dangereuse du risque d’épidémie de maladie à virus Ebola à Mayotte
- Alzheimer’s disease: from breakthroughs to real-world impact
- The impact of structural variation on Alzheimer's disease in the Alzheimer's disease sequencing project.
BibTeX
@article{rauchs2026liens,
title = {{Liens entre sommeil et maladie d’Alzheimer : impact du sexe féminin}},
author = {Géraldine Rauchs and Laura Stankeviciute and Maéva Boulin and Blandine Montagne and Claire André},
journal = {Médecine du sommeil},
year = {2026},
month = aug,
doi = {10.1016/j.msom.2026.06.004},
url = {https://hal.science/hal-05733034v1},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Liens entre sommeil et maladie d’Alzheimer : impact du sexe féminin
AU - Géraldine Rauchs
AU - Laura Stankeviciute
AU - Maéva Boulin
AU - Blandine Montagne
AU - Claire André
PY - 2026
DA - 2026/08/31
JO - Médecine du sommeil
DO - 10.1016/j.msom.2026.06.004
UR - https://hal.science/hal-05733034v1
AB - The leading cause of dementia is Alzheimer’s disease (AD). AD disproportionately affects women, a difference that cannot be explained solely by longer life expectancy but rather reflects sex-dependent biological mechanisms. In recent years, sleep disturbances have emerged as a potential modifiable risk factor for AD, as they appear early in the disease course – often preceding cognitive symptoms – and are associated with the accumulation of amyloid and tau pathology. This narrative review synthesizes evidence from human studies examining the influence of biological sex on the relationship between sleep and AD, with a particular focus on obstructive sleep apnea, insomnia, alterations in sleep architecture and microstructure, and circadian rhythm disturbances. A growing body of literature suggests that women may be more vulnerable to the neurocognitive consequences of sleep disturbances, particularly around the menopausal transition, a period characterized by profound hormonal changes that may interact with neurodegenerative processes. Despite this emerging evidence, studies explicitly integrating biological sex, hormonal status, and their interactions with sleep remain very scarce, with some findings showing heterogeneity. This review highlights the need for future research incorporating such data, using stratified and longitudinal designs, to improve our understanding of the mechanisms linking sleep and AD, and to optimize personalized prevention and management strategies for AD.
SN - 1769-4493
ER -