[Sleep and dementia].

Schlaf und Demenz.
Alzheimer’s disease Amyloid beta Mild cognitive impairment Orexin Tau protein

Journal

Zeitschrift fur Gerontologie und Geriatrie
ISSN: 1435-1269
Titre abrégé: Z Gerontol Geriatr
Pays: Germany
ID NLM: 9506215

Informations de publication

Date de publication:
Nov 2023
Historique:
accepted: 10 08 2023
pubmed: 7 9 2023
medline: 7 9 2023
entrez: 7 9 2023
Statut: ppublish

Résumé

Aging is associated with changes in sleep structure and cerebral deposition of amyloid beta and tau proteins. Sleep disturbances precede the onset of dementia by years. Comorbid sleep disorders, such as insomnia and sleep-disordered breathing, a family history of dementia and epigenetic factors can contribute to the development of dementia. This article explores the question of the interaction between sleep and dementia based on the existing literature. Alterations caused by slow wave sleep lead to changes in the glymphatic clearance of amyloid beta, tau proteins and other proteins. Transient and chronic sleep disorders cause disturbances in the brain areas responsible for cognition and behavior. Sleep-regulating brain areas are the first to be affected in the neurodegenerative process and accelerate the risk of dementia. Circadian age-related changes in amyloid beta and tau proteins affect the amount and depth of sleep and vice versa. Amyloid beta in cerebrospinal fluid shows an inverse correlation with sleep. Orexins modulate amyloid beta and sleep. Altern geht mit Änderungen der Schlafstruktur sowie zerebraler Ablagerung von Amyloid‑β und Tau-Proteinen einher. Schlafstörungen gehen dem Beginn einer Demenz um Jahre voraus. Komorbide Schlafstörungen wie Insomnien und schlafbezogene Atmungsstörungen, familiäre Demenzbelastung und epigenetische Faktoren können zur Demenzentwicklung beitragen. Dieser Beitrag geht der Frage nach der Interaktion zwischen Schlaf und Demenz anhand von bisher existierender Literatur nach. Veränderungen von „slow wave sleep“ führen zu Änderungen der glymphatischen Clearance von Amyloid‑β, Tau- und anderen Proteinen. Transiente und chronifizierte Schlafstörungen verursachen Veränderungen in Gehirnarealen, die für Kognition und Verhalten verantwortlich sind. Schlafregulierende Hirnareale sind als erste im neurodegenerativen Prozess betroffen und beschleunigen das Demenzrisiko. Zirkadiane altersbedingte Änderungen von Amyloid‑β und Tau-Protein beeinflussen die Schlafmenge bzw. -tiefe und umgekehrt. Die Liquor-Aβ-Konzentration weist eine inverse Korrelation mit dem Schlaf auf. Orexine modulieren Amyloid‑β und Schlaf.

Autres résumés

Type: Publisher (ger)
Altern geht mit Änderungen der Schlafstruktur sowie zerebraler Ablagerung von Amyloid‑β und Tau-Proteinen einher. Schlafstörungen gehen dem Beginn einer Demenz um Jahre voraus. Komorbide Schlafstörungen wie Insomnien und schlafbezogene Atmungsstörungen, familiäre Demenzbelastung und epigenetische Faktoren können zur Demenzentwicklung beitragen. Dieser Beitrag geht der Frage nach der Interaktion zwischen Schlaf und Demenz anhand von bisher existierender Literatur nach. Veränderungen von „slow wave sleep“ führen zu Änderungen der glymphatischen Clearance von Amyloid‑β, Tau- und anderen Proteinen. Transiente und chronifizierte Schlafstörungen verursachen Veränderungen in Gehirnarealen, die für Kognition und Verhalten verantwortlich sind. Schlafregulierende Hirnareale sind als erste im neurodegenerativen Prozess betroffen und beschleunigen das Demenzrisiko. Zirkadiane altersbedingte Änderungen von Amyloid‑β und Tau-Protein beeinflussen die Schlafmenge bzw. -tiefe und umgekehrt. Die Liquor-Aβ-Konzentration weist eine inverse Korrelation mit dem Schlaf auf. Orexine modulieren Amyloid‑β und Schlaf.

Identifiants

pubmed: 37676320
doi: 10.1007/s00391-023-02237-5
pii: 10.1007/s00391-023-02237-5
doi:

Types de publication

English Abstract Journal Article Review

Langues

ger

Sous-ensembles de citation

IM

Pagination

556-560

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.

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Auteurs

Geert Mayer (G)

Philipps-Universität Marburg, Marburg, Deutschland. geert.mayer@t-online.de.
, Privatweg 2, 34582, Borken, Deutschland. geert.mayer@t-online.de.

Carla Stenmanns (C)

Klinik für Orthopädie und Unfallchirurgie, Altersmedizin, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Deutschland.

Thorsten R Doeppner (TR)

Klinik für Neurologie, Universitätsklinkum Gießen und Marburg, Gießen, Deutschland.

Dirk M Hermann (DM)

Klinik für Neurologie, Universitätsklinikum Essen, Essen, Deutschland.

Janine Gronewold (J)

Klinik für Neurologie, Universitätsklinikum Essen, Essen, Deutschland.

Classifications MeSH