TY - JOUR
T1 - Basal forebrain metabolism in Alzheimer's disease continuum
T2 - relationship with education
AU - Alzheimer's Disease Neuroimaging Initiative
AU - Nicolas, Brandt
AU - Alessandra, Dodich
AU - Daniela, Perani
AU - Osman, Ratib
AU - Sara, Trombella
AU - Giovanni B, Frisoni
AU - Valentina, Garibotto
N1 - Funding Information:
VG, AD, and GBF were funded by a grant from the Swiss National Science Foundation (SNF 320030_169876 ). VG was funded by a grant of the Velux Foundation (project 1123 ).
Funding Information:
The data repository and collection of the data used for these analyses were funded as an ADNI by a National Institutes of Health grant (U01 AG024904) and a Department of Defense ADNI (Department of Defense award No. W81XWH-12-2?0012). The ADNI is funded by the National Institute on Aging and the National Institute of Biomedical Imaging and Bioengineering and through contributions from: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai, Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche, Ltd. and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO, Ltd.; Janssen Alzheimer Immunotherapy Research and Development, LLC.; Johnson and Johnson Pharmaceutical Research and Development LLC.; Lumosity; Lundbeck; Merck and Co. Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer, Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research provides funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and this study was coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory of Neuro Imaging at the University of Southern California. VG, AD, and GBF were funded by a grant from the Swiss National Science Foundation (SNF 320030_169876). VG was funded by a grant of the Velux Foundation (project 1123).
Funding Information:
The data repository and collection of the data used for these analyses were funded as an ADNI by a National Institutes of Health grant ( U01 AG024904 ) and a Department of Defense ADNI (Department of Defense award No. W81XWH-12-2–0012 ). The ADNI is funded by the National Institute on Aging and the National Institute of Biomedical Imaging and Bioengineering and through contributions from: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai, Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche, Ltd., and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO, Ltd.; Janssen Alzheimer Immunotherapy Research and Development, LLC.; Johnson and Johnson Pharmaceutical Research and Development LLC.; Lumosity; Lundbeck; Merck and Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer, Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research provides funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health ( www.fnih.org ). The grantee organization is the Northern California Institute for Research and Education, and this study was coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory of Neuro Imaging at the University of Southern California.
Publisher Copyright:
© 2019 Elsevier Inc.
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2020/3
Y1 - 2020/3
N2 - We analyzed education, as a proxy of cognitive reserve, and the cholinergic pathway in Alzheimer's disease (AD), to test the hypothesis that education might modulate the relationship between clinical symptoms and metabolic and structural changes in AD. We included 84 subjects and compared between diagnostic groups and different educational levels the glucose metabolism of basal forebrain (BFM) and volume of the basal forebrain, the major cholinergic structure, and hippocampus (HM) (and hippocampal volume), a relevant projection site for the basal forebrain. Correlations with the global cognitive status and education in the whole sample were also performed. Patients with AD dementia showed reduced basal forebrain volume, hippocampal volume, and HM compared with controls. In the whole group, the global cognitive status was positively correlated with BFM and HM. Among high-educated subjects, mild cognitive impairment showed higher BFM and HM in comparison to other diagnostic groups. Our results suggest that in mild cognitive impairment subjects with a higher educational level, cholinergic activity is upregulated and this appears to have a compensatory effect, which may be lost in later symptomatic stages.
AB - We analyzed education, as a proxy of cognitive reserve, and the cholinergic pathway in Alzheimer's disease (AD), to test the hypothesis that education might modulate the relationship between clinical symptoms and metabolic and structural changes in AD. We included 84 subjects and compared between diagnostic groups and different educational levels the glucose metabolism of basal forebrain (BFM) and volume of the basal forebrain, the major cholinergic structure, and hippocampus (HM) (and hippocampal volume), a relevant projection site for the basal forebrain. Correlations with the global cognitive status and education in the whole sample were also performed. Patients with AD dementia showed reduced basal forebrain volume, hippocampal volume, and HM compared with controls. In the whole group, the global cognitive status was positively correlated with BFM and HM. Among high-educated subjects, mild cognitive impairment showed higher BFM and HM in comparison to other diagnostic groups. Our results suggest that in mild cognitive impairment subjects with a higher educational level, cholinergic activity is upregulated and this appears to have a compensatory effect, which may be lost in later symptomatic stages.
KW - Alzheimer's disease (AD)
KW - Basal forebrain
KW - Education
KW - Fluorodeoxyglucose (FDG)
KW - Positron emission tomography (PET)
KW - Reserve
UR - http://www.scopus.com/inward/record.url?scp=85078722983&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85078722983&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2019.11.013
DO - 10.1016/j.neurobiolaging.2019.11.013
M3 - Article
C2 - 32008856
AN - SCOPUS:85078722983
VL - 87
SP - 70
EP - 77
JO - Neurobiology of Aging
JF - Neurobiology of Aging
SN - 0197-4580
ER -