Regional Neocortical Gray Matter Structure and Sleep Fragmentation in Older Adults.
OBJECTIVE
To test the hypothesis that greater sleep fragmentation is associated with regionally decreased cortical gray matter volume in older community-dwelling adults without cognitive impairment.


METHODS
We studied 141 community-dwelling older adults (median age 82.9; 73% female) without cognitive impairment or stroke, and not using sedative/ hypnotic medications, participating in the Rush Memory and Aging Project. We quantified sleep fragmentation from 7 d of actigraphy using the metric kRA and related this to total cortical gray matter volume, and regional gray matter volume in 34 cortical regions quantified by automated segmentation of magnetic resonance imaging data. We determined statistical significance and accounted for multiple comparisons by empirically estimating the false discovery rate by permutation.


RESULTS
Lower total cortical gray matter volume was associated with higher sleep fragmentation (coefficient +0.23, standard error [SE] 0.11, P = 0.037). Lower gray matter volumes in four cortical regions were accompanied by higher sleep fragmentation with a false discovery rate < 0.05: the left (coefficient +0.36, SE 0.10, P = 2.7 × 10(-4)) and right (coefficient +0.31, SE 0.10, P = 4.0 × 10(-3)) lateral orbitofrontal cortices, and the adjacent left (coefficient +0.31, SE 0.10, 5.4 × 10(-4)) and right (coefficient +0.39, SE 0.10, P = 1.2 × 10(-4)) inferior frontal gyri pars orbitalis. These associations were unchanged after accounting for age, sex, education, depression, cognitive function, and a number of medical comorbidities.


CONCLUSIONS
Lower cortical gray matter volume in the lateral orbitofrontal cortex and inferior frontal gyrus pars orbitalis is associated with greater sleep fragmentation in older community-dwelling adults. Further work is needed to clarify whether this is a consequence of or contributor to sleep fragmentation.


CONCLUSIONS
A commentary on this article appears in this issue on page 15.
Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada.
Andrew S P
AS
Lim
Rush Alzheimer Disease Center and Department of Neurological Sciences, Rush University, Chicago, IL.
Debra A
DA
Fleischman
Rush Alzheimer Disease Center and Department of Neurological Sciences, Rush University, Chicago, IL.|Department of Diagnostic Radiology and Nuclear Medicine, Rush University Medical Center, Chicago, IL.
Robert J
RJ
Dawe
Rush Alzheimer Disease Center and Department of Neurological Sciences, Rush University, Chicago, IL.
Lei
L
Yu
Rush Alzheimer Disease Center and Department of Neurological Sciences, Rush University, Chicago, IL.|Department of Diagnostic Radiology and Nuclear Medicine, Rush University Medical Center, Chicago, IL.|Department of Biomedical Engineering, Illinois Institute of Technology, Chicago, IL.
Konstantinos
K
Arfanakis
Rush Alzheimer Disease Center and Department of Neurological Sciences, Rush University, Chicago, IL.
Aron S
AS
Buchman
Rush Alzheimer Disease Center and Department of Neurological Sciences, Rush University, Chicago, IL.
David A
DA
Bennett
D056044:Actigraphy; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging; D003071:Cognition; D003072:Cognition Disorders; D003863:Depression / Q000453:epidemiology; D005260:Female; D066128:Gray Matter / Q000473:pathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008568:Memory; D019579:Neocortex / Q000473:pathology*; D017397:Prefrontal Cortex / Q000473:pathology; D012890:Sleep; D012892:Sleep Deprivation / Q000453:epidemiology / Q000473:pathology*; D020521:Stroke
actigraphy; aging; magnetic resonance imaging; orbitofrontal cortex; sleep fragmentation