Medial temporal lobe atrophy relates more strongly to sleep-wake rhythm fragmentation than to age or any other known risk

Eus J.W. Van Someren, J. M. Oosterman, B. Van Harten, R. L. Vogels, A. A. Gouw, H. C. Weinstein, A. Poggesi, Ph Scheltens, E. J.A. Scherder

Research output: Contribution to JournalArticleAcademicpeer-review

Abstract

Atrophy of the medial temporal lobe of the brain is key to memory function and memory complaints in old age. While age and some morbidities are major risk factors for medial temporal lobe atrophy, individual differences remain, and mechanisms are insufficiently known. The largest combined neuroimaging and whole genome study to date indicates that medial temporal lobe volume is most associated with common polymorphisms in the GRIN2B gene that encodes for the 2B subunit (NR2B) of the NMDA receptor. Because sleep disruption induces a selective loss of NR2B from hippocampal synaptic membranes in rodents, and because of several other reports on medial temporal lobe sensitivity to sleep disruption, we hypothesized a contribution of the typical age-related increase in sleep-wake rhythm fragmentation to medial temporal lobe atrophy. Magnetic resonance imaging and actigraphy in 138 aged individuals showed that individual differences in sleep-wake rhythm fragmentation accounted for more (19%) of the variance in medial temporal lobe atrophy than age did (15%), or any of a list of health and brain structural indicators. The findings suggest a role of sleep-wake rhythm fragmentation in age-related medial temporal lobe atrophy, that might in part be prevented or reversible.

Original languageEnglish
Pages (from-to)1-7
Number of pages7
JournalNeurobiology of Learning and Memory
DOIs
Publication statusE-pub ahead of print - 1 Jun 2018

Fingerprint

Temporal Lobe
Atrophy
Sleep
Individuality
Actigraphy
Synaptic Membranes
Brain
Neuroimaging
Rodentia
Magnetic Resonance Imaging
Genome
Morbidity
Health
Genes

Keywords

  • Aging
  • Circadian rhythm
  • Medial temporal lobe atrophy
  • Neurodegeneration
  • Physical activity
  • Rhythm fragmentation
  • Sleep

Cite this

Van Someren, Eus J.W. ; Oosterman, J. M. ; Van Harten, B. ; Vogels, R. L. ; Gouw, A. A. ; Weinstein, H. C. ; Poggesi, A. ; Scheltens, Ph ; Scherder, E. J.A. / Medial temporal lobe atrophy relates more strongly to sleep-wake rhythm fragmentation than to age or any other known risk. In: Neurobiology of Learning and Memory. 2018 ; pp. 1-7.
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abstract = "Atrophy of the medial temporal lobe of the brain is key to memory function and memory complaints in old age. While age and some morbidities are major risk factors for medial temporal lobe atrophy, individual differences remain, and mechanisms are insufficiently known. The largest combined neuroimaging and whole genome study to date indicates that medial temporal lobe volume is most associated with common polymorphisms in the GRIN2B gene that encodes for the 2B subunit (NR2B) of the NMDA receptor. Because sleep disruption induces a selective loss of NR2B from hippocampal synaptic membranes in rodents, and because of several other reports on medial temporal lobe sensitivity to sleep disruption, we hypothesized a contribution of the typical age-related increase in sleep-wake rhythm fragmentation to medial temporal lobe atrophy. Magnetic resonance imaging and actigraphy in 138 aged individuals showed that individual differences in sleep-wake rhythm fragmentation accounted for more (19{\%}) of the variance in medial temporal lobe atrophy than age did (15{\%}), or any of a list of health and brain structural indicators. The findings suggest a role of sleep-wake rhythm fragmentation in age-related medial temporal lobe atrophy, that might in part be prevented or reversible.",
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Medial temporal lobe atrophy relates more strongly to sleep-wake rhythm fragmentation than to age or any other known risk. / Van Someren, Eus J.W.; Oosterman, J. M.; Van Harten, B.; Vogels, R. L.; Gouw, A. A.; Weinstein, H. C.; Poggesi, A.; Scheltens, Ph; Scherder, E. J.A.

In: Neurobiology of Learning and Memory, 01.06.2018, p. 1-7.

Research output: Contribution to JournalArticleAcademicpeer-review

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