TY - JOUR
T1 - Cerebrovascular disease, neurodegeneration, and clinical phenotype in dementia with Lewy bodies
AU - Ferreira, Daniel
AU - Nedelska, Zuzana
AU - Graff-Radford, Jonathan
AU - Przybelski, Scott A.
AU - Lesnick, Timothy G.
AU - Schwarz, Christopher G.
AU - Botha, Hugo
AU - Senjem, Matthew L.
AU - Fields, Julie A.
AU - Knopman, David S.
AU - Savica, Rodolfo
AU - Ferman, Tanis J.
AU - Graff-Radford, Neill R.
AU - Lowe, Val J.
AU - Jack, Clifford R.
AU - Petersen, Ronald C.
AU - Lemstra, Afina W.
AU - van de Beek, Marleen
AU - Barkhof, Frederik
AU - Blanc, Frederic
AU - Loureiro de Sousa, Paulo
AU - Philippi, Nathalie
AU - Cretin, Benjamin
AU - Demuynck, Catherine
AU - Hort, Jakub
AU - Oppedal, Ketil
AU - Boeve, Bradley F.
AU - Aarsland, Dag
AU - Westman, Eric
AU - Kantarci, Kejal
N1 - Funding Information:
The authors particularly thank the patients and their family members for participating in this research. This work was supported by the National Institutes of Health ( U01- NS100620, P50-AG016574, U01-AG006786, R37-AG011378, R01-AG041851, R01-AG040042, C06-RR018898 and R01-NS080820 ), Foundation Dr. Corinne Schuler, the Mangurian Foundation for Lewy Body Research, the Elsie and Marvin Dekelboum Family Foundation, the Little Family Foundation, the Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program, the Western Norway Regional Health Authority, the Swedish Foundation for Strategic Research (SSF), the Swedish Research Council (VR), Karolinska Institutet travel grants, Center for Innovative Medicine (CIMED), the Foundation for Geriatric Diseases at Karolinska Institutet, the NIHR biomedical research centre at UCLH, and the Projet Hospitalier de Recherche Clinique ( PHRC, IDCRB 2012-A00992-41 ) and fondation Université de Strasbourg. The sponsors played no role in study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.
Funding Information:
The authors particularly thank the patients and their family members for participating in this research. This work was supported by the National Institutes of Health (U01- NS100620, P50-AG016574, U01-AG006786, R37-AG011378, R01-AG041851, R01-AG040042, C06-RR018898 and R01-NS080820), Foundation Dr. Corinne Schuler, the Mangurian Foundation for Lewy Body Research, the Elsie and Marvin Dekelboum Family Foundation, the Little Family Foundation, the Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program, the Western Norway Regional Health Authority, the Swedish Foundation for Strategic Research (SSF), the Swedish Research Council (VR), Karolinska Institutet travel grants, Center for Innovative Medicine (CIMED), the Foundation for Geriatric Diseases at Karolinska Institutet, the NIHR biomedical research centre at UCLH, and the Projet Hospitalier de Recherche Clinique (PHRC, IDCRB 2012-A00992-41) and fondation Universit? de Strasbourg. The sponsors played no role in study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.
Publisher Copyright:
© 2021 Elsevier Inc.
PY - 2021/9
Y1 - 2021/9
N2 - We investigated whether cerebrovascular disease contributes to neurodegeneration and clinical phenotype in dementia with Lewy bodies (DLB). Regional cortical thickness and subcortical gray matter volumes were estimated from structural magnetic resonance imaging (MRI) in 165 DLB patients. Cortical and subcortical infarcts were recorded and white matter hyperintensities (WMHs) were assessed. Subcortical only infarcts were more frequent (13.3%) than cortical only infarcts (3.1%) or both subcortical and cortical infarcts (2.4%). Infarcts, irrespective of type, were associated with WMHs. A higher WMH volume was associated with thinner orbitofrontal, retrosplenial, and posterior cingulate cortices, smaller thalamus and pallidum, and larger caudate volume. A higher WMH volume was associated with the presence of visual hallucinations and lower global cognitive performance, and tended to be associated with the absence of probable rapid eye movement sleep behavior disorder. Presence of infarcts was associated with the absence of parkinsonism. We conclude that cerebrovascular disease is associated with gray matter neurodegeneration in patients with probable DLB, which may have implications for the multifactorial treatment of probable DLB.
AB - We investigated whether cerebrovascular disease contributes to neurodegeneration and clinical phenotype in dementia with Lewy bodies (DLB). Regional cortical thickness and subcortical gray matter volumes were estimated from structural magnetic resonance imaging (MRI) in 165 DLB patients. Cortical and subcortical infarcts were recorded and white matter hyperintensities (WMHs) were assessed. Subcortical only infarcts were more frequent (13.3%) than cortical only infarcts (3.1%) or both subcortical and cortical infarcts (2.4%). Infarcts, irrespective of type, were associated with WMHs. A higher WMH volume was associated with thinner orbitofrontal, retrosplenial, and posterior cingulate cortices, smaller thalamus and pallidum, and larger caudate volume. A higher WMH volume was associated with the presence of visual hallucinations and lower global cognitive performance, and tended to be associated with the absence of probable rapid eye movement sleep behavior disorder. Presence of infarcts was associated with the absence of parkinsonism. We conclude that cerebrovascular disease is associated with gray matter neurodegeneration in patients with probable DLB, which may have implications for the multifactorial treatment of probable DLB.
KW - Cerebrovascular disease
KW - Dementia with Lewy bodies (DLB)
KW - Magnetic resonance imaging
KW - Neurodegeneration
KW - White matter hyperintensities
KW - infarcts
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UR - http://www.scopus.com/inward/citedby.url?scp=85107763909&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2021.04.029
DO - 10.1016/j.neurobiolaging.2021.04.029
M3 - Article
C2 - 34130107
AN - SCOPUS:85107763909
SN - 0197-4580
VL - 105
SP - 252
EP - 261
JO - Neurobiology of Aging
JF - Neurobiology of Aging
ER -