TY - JOUR
T1 - Pattern of regional white matter hyperintensity volume in mild cognitive impairment subtypes and associations with decline in daily functioning
AU - Alzheimer’s Disease Neuroimaging Initiative
AU - Bangen, Katherine J.
AU - Thomas, Kelsey R.
AU - Weigand, Alexandra J.
AU - Sanchez, Danielle L.
AU - Delano-Wood, Lisa
AU - Edmonds, Emily C.
AU - Carmichael, Owen T.
AU - Schwarz, Christopher G.
AU - Brickman, Adam M.
AU - Bondi, Mark W.
N1 - Funding Information:
Sources of funding for this project include VA Clinical Science Research & Development (Career Development Award-2 1IK2CX000938 to KJB and 1IK2CX001415 to E.C.E.); Alzheimer's Association ( AARF-17-528918 to K.R.T. , AARG-18-566254 to K.J.B. , and AARG-17-500358 to E.C.E. ); grants from the National Institutes of Health ( National Institute on Aging R01 AG049810 and K24 AG026431 to M.W.B . and San Diego State University Advancing Diversity in Aging Research Program [R25AG043364]); and the Dana Foundation (to K.J.B.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Data collection and sharing for this project was funded by the Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2–0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: 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 & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & 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 is providing 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 the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. Appendix A
Funding Information:
Sources of funding for this project include VA Clinical Science Research & Development (Career Development Award-2 1IK2CX000938 to KJB and 1IK2CX001415 to E.C.E.); Alzheimer's Association (AARF-17-528918 to K.R.T., AARG-18-566254 to K.J.B., and AARG-17-500358 to E.C.E.); grants from the National Institutes of Health (National Institute on Aging R01 AG049810 and K24 AG026431 to M.W.B. and San Diego State University Advancing Diversity in Aging Research Program [R25AG043364]); and the Dana Foundation (to K.J.B.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Data collection and sharing for this project was funded by the Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2–0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: 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 & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & 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 is providing 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 the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California.
Publisher Copyright:
© 2019
PY - 2020/2
Y1 - 2020/2
N2 - White matter hyperintensities (WMHs), a marker of small-vessel cerebrovascular disease, increase risk for mild cognitive impairment (MCI). Less is known about whether regional WMHs distinguish MCI subtypes and predict decline in everyday functioning. About 618 Alzheimer's Disease Neuroimaging Initiative participants (301 cognitively normal [CN]; 232 amnestic MCI [aMCI]; 85 nonamnestic MCI [naMCI]) underwent neuropsychological testing, MRI, and assessment of everyday functioning. aMCI participants showed greater temporal (p = 0.002) and occipital WMHs (p = 0.030) relative to CN whereas naMCI participants had greater frontal (p = 0.045), temporal (p = 0.003), parietal (p = 0.018), and occipital (p < 0.001) WMH compared with CN. Relative to those with aMCI, individuals with naMCI showed greater occipital WMH (p = 0.013). Greater WMH in temporal (p = 0.001) and occipital regions (p = 0.006) was associated with faster decline in everyday functioning across the sample. Temporal lobe WMHs were disproportionately associated with accelerated functional decline among naMCI (p = 0.045). Regional WMH volumes vary across cognitive groups and predict functional decline. Cerebrovascular markers may help identify individuals at risk for decline and distinguish subtypes of cognitive impairment.
AB - White matter hyperintensities (WMHs), a marker of small-vessel cerebrovascular disease, increase risk for mild cognitive impairment (MCI). Less is known about whether regional WMHs distinguish MCI subtypes and predict decline in everyday functioning. About 618 Alzheimer's Disease Neuroimaging Initiative participants (301 cognitively normal [CN]; 232 amnestic MCI [aMCI]; 85 nonamnestic MCI [naMCI]) underwent neuropsychological testing, MRI, and assessment of everyday functioning. aMCI participants showed greater temporal (p = 0.002) and occipital WMHs (p = 0.030) relative to CN whereas naMCI participants had greater frontal (p = 0.045), temporal (p = 0.003), parietal (p = 0.018), and occipital (p < 0.001) WMH compared with CN. Relative to those with aMCI, individuals with naMCI showed greater occipital WMH (p = 0.013). Greater WMH in temporal (p = 0.001) and occipital regions (p = 0.006) was associated with faster decline in everyday functioning across the sample. Temporal lobe WMHs were disproportionately associated with accelerated functional decline among naMCI (p = 0.045). Regional WMH volumes vary across cognitive groups and predict functional decline. Cerebrovascular markers may help identify individuals at risk for decline and distinguish subtypes of cognitive impairment.
KW - Cerebrovascular disease
KW - Daily functioning
KW - MCI subtypes
KW - Mild cognitive impairment
KW - Neuropsychology
KW - White matter hyperintensity
UR - http://www.scopus.com/inward/record.url?scp=85076233492&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85076233492&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2019.10.016
DO - 10.1016/j.neurobiolaging.2019.10.016
M3 - Article
C2 - 31791658
AN - SCOPUS:85076233492
SN - 0197-4580
VL - 86
SP - 134
EP - 142
JO - Neurobiology of Aging
JF - Neurobiology of Aging
ER -