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@ARTICLE{JosephMathurin:155387,
author = {Joseph-Mathurin, Nelly and Wang, Guoqiao and Kantarci,
Kejal and Jack, Clifford R and McDade, Eric and Hassenstab,
Jason and Blazey, Tyler M and Gordon, Brian A and Su, Yi and
Chen, Gengsheng and Massoumzadeh, Parinaz and Hornbeck, Russ
C and Allegri, Ricardo F and Ances, Beau M and Berman, Sarah
B and Brickman, Adam M and Brooks, William S and Cash, David
M and Chhatwal, Jasmeer P and Chui, Helena C and Correia,
Stephen and Cruchaga, Carlos and Farlow, Martin R and Fox,
Nick C and Fulham, Michael and Ghetti, Bernardino and
Graff-Radford, Neill R and Johnson, Keith A and Karch,
Celeste M and Laske, Christoph and Lee, Athene K W and
Levin, Johannes and Masters, Colin L and Noble, James M and
O'Connor, Antoinette and Perrin, Richard J and Preboske,
Gregory M and Ringman, John M and Rowe, Christopher C and
Salloway, Stephen and Saykin, Andrew J and Schofield, Peter
R and Shimada, Hiroyuki and Shoji, Mikio and Suzuki, Kazushi
and Villemagne, Victor L and Xiong, Chengjie and Yakushev,
Igor and Morris, John C and Bateman, Randall J and
Benzinger, Tammie L S},
collaboration = {Network, Dominantly Inherited Alzheimer},
title = {{L}ongitudinal {A}ccumulation of {C}erebral
{M}icrohemorrhages in {D}ominantly {I}nherited {A}lzheimer
{D}isease.},
journal = {Neurology},
volume = {96},
number = {12},
issn = {1526-632X},
address = {[S.l.]},
publisher = {Ovid},
reportid = {DZNE-2021-00627},
pages = {e1632 - e1645},
year = {2021},
abstract = {To investigate the inherent clinical risks associated with
the presence of cerebral microhemorrhages (CMHs) or cerebral
microbleeds and characterize individuals at high risk for
developing hemorrhagic amyloid-related imaging abnormality
(ARIA-H), we longitudinally evaluated families with
dominantly inherited Alzheimer disease (DIAD).Mutation
carriers (n = 310) and noncarriers (n = 201) underwent
neuroimaging, including gradient echo MRI sequences to
detect CMHs, and neuropsychological and clinical
assessments. Cross-sectional and longitudinal analyses
evaluated relationships between CMHs and neuroimaging and
clinical markers of disease.Three percent of noncarriers and
$8\%$ of carriers developed CMHs primarily located in lobar
areas. Carriers with CMHs were older, had higher diastolic
blood pressure and Hachinski ischemic scores, and more
clinical, cognitive, and motor impairments than those
without CMHs. APOE ε4 status was not associated with the
prevalence or incidence of CMHs. Prevalent or incident CMHs
predicted faster change in Clinical Dementia Rating although
not composite cognitive measure, cortical thickness,
hippocampal volume, or white matter lesions. Critically, the
presence of 2 or more CMHs was associated with a significant
risk for development of additional CMHs over time (8.95 ±
10.04 per year).Our study highlights factors associated with
the development of CMHs in individuals with DIAD. CMHs are a
part of the underlying disease process in DIAD and are
significantly associated with dementia. This highlights that
in participants in treatment trials exposed to drugs, which
carry the risk of ARIA-H as a complication, it may be
challenging to separate natural incidence of CMHs from
drug-related CMHs.},
keywords = {Adult / Alzheimer Disease: complications / Alzheimer
Disease: pathology / Brain: pathology / Cerebral Hemorrhage:
epidemiology / Cerebral Hemorrhage: etiology / Cerebral
Hemorrhage: pathology / Female / Humans / Longitudinal
Studies / Magnetic Resonance Imaging / Male / Middle Aged},
cin = {Core ICRU / Clinical Dementia Research München / München
common},
ddc = {610},
cid = {I:(DE-2719)1240005 / I:(DE-2719)1111016 /
I:(DE-2719)6000016},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33495373},
pmc = {pmc:PMC8032370},
doi = {10.1212/WNL.0000000000011542},
url = {https://pub.dzne.de/record/155387},
}