Gray matter network disruptions and amyloid beta in cognitively normal adults

Betty M. Tijms, Mara ten Kate, Alle Meije Wink, Pieter Jelle Visser, Mirian Ecay, Montserrat Clerigue, Ainara Estanga, Maite Garcia Sebastian, Andrea Izagirre, Jorge Villanua, Pablo Martinez Lage, Wiesje M. van der Flier, Philip Scheltens, Ernesto Sanz Arigita, Frederik Barkhof
Neurobiology of Aging. 2016-01-01; 37: 154-160
DOI: 10.1016/j.neurobiolaging.2015.10.015

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1. Neurobiol Aging. 2016 Jan;37:154-160. doi: 10.1016/j.neurobiolaging.2015.10.015.
Epub 2015 Oct 22.

Gray matter network disruptions and amyloid beta in cognitively normal adults.

Tijms BM(1), Kate MT(2), Wink AM(3), Visser PJ(4), Ecay M(5), Clerigue M(5),
Estanga A(5), Garcia Sebastian M(5), Izagirre A(5), Villanua J(6), Martinez Lage
P(5), van der Flier WM(7), Scheltens P(8), Sanz Arigita E(5), Barkhof F(3).

Author information:
(1)Alzheimer Center and Department of Neurology, Neuroscience Campus Amsterdam,
VU University Medical Center, Amsterdam, the Netherlands. Electronic address:
.
(2)Alzheimer Center and Department of Neurology, Neuroscience Campus Amsterdam,
VU University Medical Center, Amsterdam, the Netherlands; Department of Radiology
and Nuclear Medicine, Neuroscience Campus Amsterdam, VU University Medical
Center, Amsterdam, the Netherlands.
(3)Department of Radiology and Nuclear Medicine, Neuroscience Campus Amsterdam,
VU University Medical Center, Amsterdam, the Netherlands.
(4)Alzheimer Center and Department of Neurology, Neuroscience Campus Amsterdam,
VU University Medical Center, Amsterdam, the Netherlands; Department of
Psychiatry and Neuropsychology, School for Mental Health and Neuroscience,
Maastricht University, Maastricht, the Netherlands.
(5)Department of Neurology, CITA-Alzheimer Foundation, San Sebastian, Spain.
(6)Department of Neurology, CITA-Alzheimer Foundation, San Sebastian, Spain;
Donostia Unit, Osatek SA, Donostia University Hospital, San Sebastian, Spain.
(7)Alzheimer Center and Department of Neurology, Neuroscience Campus Amsterdam,
VU University Medical Center, Amsterdam, the Netherlands; Department of
Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, the
Netherlands.
(8)Alzheimer Center and Department of Neurology, Neuroscience Campus Amsterdam,
VU University Medical Center, Amsterdam, the Netherlands.

Gray matter networks are disrupted in Alzheimer’s disease (AD). It is unclear
when these disruptions start during the development of AD. Amyloid beta 1-42
(Aβ42) is among the earliest changes in AD. We studied, in cognitively healthy
adults, the relationship between Aβ42 levels in cerebrospinal fluid (CSF) and
single-subject cortical gray matter network measures. Single-subject gray matter
networks were extracted from structural magnetic resonance imaging scans in a
sample of cognitively healthy adults (N = 185; age range 39-79, mini-mental state
examination >25, N = 12 showed abnormal Aβ42 < 550 pg/mL). Degree, clustering coefficient, and path length were computed at whole brain level and for 90 anatomical areas. Associations between continuous Aβ42 CSF levels and single-subject cortical gray matter network measures were tested. Smoothing splines were used to determine whether a linear or nonlinear relationship gave a better fit to the data. Lower Aβ42 CSF levels were linearly associated at whole brain level with lower connectivity density, and nonlinearly with lower clustering values and higher path length values, which is indicative of a less-efficient network organization. These relationships were specific to medial temporal areas, precuneus, and the middle frontal gyrus (all p < 0.05). These results suggest that mostly within the normal spectrum of amyloid, lower Aβ42 levels can be related to gray matter networks disruptions. Copyright © 2016 Elsevier Inc. All rights reserved. DOI: 10.1016/j.neurobiolaging.2015.10.015 PMID: 26559882 [Indexed for MEDLINE]

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