TY - JOUR
T1 - Left Frontal Hub Connectivity during Memory Performance Supports Reserve in Aging and Mild Cognitive Impairment
AU - Franzmeier, Nicolai
AU - Hartmann, Julia
AU - Taylor, Alexander N. W.
AU - Araque Caballero, Miguel A.
AU - Simon-Vermot, Lee
AU - Beurger, Katharina
AU - Kambeitz-Ilankovic, Lana
AU - Ertl-Wagner, Birgit
AU - Mueller, Claudia
AU - Catak, Cihan
AU - Janowitz, Daniel
AU - Stahl, Robert
AU - Dichgans, Martin
AU - Duering, Marco
AU - Ewers, Michael
N1 - Funding Information:
The studywas funded by an ERC career integration grant (PCIG12-GA-2012-334259 to ME), LMUexcellent (to ME), and Alzheimer Forschung Initiative (to MD and ME).
Publisher Copyright:
© 2017 - IOS Press and the authors.
PY - 2017/8/14
Y1 - 2017/8/14
N2 - Reserve in aging and Alzheimer’s disease (AD) is defined as maintaining cognition at a relatively high level in the presence of neurodegeneration, an ability often associated with higher education among other life factors. Recent evidence suggests that higher resting-state functional connectivity within the frontoparietal control network, specifically the left frontal cortex (LFC) hub, contributes to higher reserve. Following up these previous resting-state fMRI findings, we probed memory-task related functional connectivity of the LFC hub as a neural substrate of reserve. In elderly controls (CN, n = 37) and patients with mild cognitive impairment (MCI, n = 17), we assessed global connectivity of the LFC hub during successful face-name association learning, using generalized psychophysiological interaction analyses. Reserve was quantified as residualized memory performance, accounted for gender and proxies of neurodegeneration (age, hippocampus atrophy, and APOE genotype). We found that greater education was associated with higher LFC-connectivity in both CN and MCI during successful memory. Furthermore, higher LFC-connectivity predicted higher residualized memory (i.e., reserve). These results suggest that higher LFC-connectivity contributes to reserve in both healthy and pathological aging.
AB - Reserve in aging and Alzheimer’s disease (AD) is defined as maintaining cognition at a relatively high level in the presence of neurodegeneration, an ability often associated with higher education among other life factors. Recent evidence suggests that higher resting-state functional connectivity within the frontoparietal control network, specifically the left frontal cortex (LFC) hub, contributes to higher reserve. Following up these previous resting-state fMRI findings, we probed memory-task related functional connectivity of the LFC hub as a neural substrate of reserve. In elderly controls (CN, n = 37) and patients with mild cognitive impairment (MCI, n = 17), we assessed global connectivity of the LFC hub during successful face-name association learning, using generalized psychophysiological interaction analyses. Reserve was quantified as residualized memory performance, accounted for gender and proxies of neurodegeneration (age, hippocampus atrophy, and APOE genotype). We found that greater education was associated with higher LFC-connectivity in both CN and MCI during successful memory. Furthermore, higher LFC-connectivity predicted higher residualized memory (i.e., reserve). These results suggest that higher LFC-connectivity contributes to reserve in both healthy and pathological aging.
KW - Aging
KW - cognitive reserve
KW - education
KW - Functional connectivity
KW - memory
KW - mild cognitive impairment
KW - task-fMRI
KW - functional connectivity
KW - Apolipoproteins E/genetics
KW - Frontal Lobe/diagnostic imaging
KW - Humans
KW - Male
KW - Nerve Net/diagnostic imaging
KW - Aging/pathology
KW - Names
KW - Memory/physiology
KW - Aged, 80 and over
KW - Female
KW - Face
KW - Functional Laterality/physiology
KW - Neural Pathways/diagnostic imaging
KW - Magnetic Resonance Imaging
KW - Image Processing, Computer-Assisted
KW - Sex Factors
KW - Brain Mapping
KW - Pattern Recognition, Visual/physiology
KW - Aged
KW - Cognitive Dysfunction/diagnostic imaging
UR - http://www.scopus.com/inward/record.url?scp=85027158269&partnerID=8YFLogxK
U2 - 10.3233/JAD-170360
DO - 10.3233/JAD-170360
M3 - Article
C2 - 28731448
SN - 1387-2877
VL - 59
SP - 1381
EP - 1392
JO - Journal of Alzheimer’s Disease
JF - Journal of Alzheimer’s Disease
IS - 4
ER -
