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@ARTICLE{Iordanishvili:864417,
author = {Iordanishvili, Elene and Schall, Melissa and Loução,
Ricardo and Zimmermann, Markus and Kotetishvili, Ketevan and
Shah, N. Jon and Oros-Peusquens, Ana-Maria},
title = {{Q}uantitative {MRI} of cerebral white matter
hyperintensities: {A} new approach towards understanding the
underlying pathology},
journal = {NeuroImage},
volume = {202},
issn = {1053-8119},
address = {Orlando, Fla.},
publisher = {Academic Press},
reportid = {FZJ-2019-04201},
pages = {116077 -},
year = {2019},
abstract = {Interest in white matter hyperintensities (WMH), a
radiological biomarker of small vessel disease, is
continuously increasing. This is, in most part, due to our
better understanding of their association with various
clinical disorders, such as stroke and Alzheimer’s
disease, and the overlapping pathology of WMH with these
afflictions. Although post-mortem histological studies have
reported various underlying pathophysiological substrates,
in vivo research has not been specific enough to fully
corroborate these findings. Furthermore, post-mortem studies
are not able to capture which pathological processes are the
driving force of the WMH severity. The current study
attempts to fill this gap by non-invasively investigating
the influence of WMH on brain tissue using quantitative MRI
(qMRI) measurements of the water content (H2O), the
longitudinal (T1) and effective transverse relaxation times
(T2∗), as well as the semi-quantitative magnetization
transfer ratio (MTR), and bound proton fraction (ƒbound).
In total, seventy subjects (age range 50–80 years) were
selected from a population-based aging cohort study,
1000BRAINS. Normal appearing grey (NAGM) and white matter
(NAWM), as well as deep (DWMH) and periventricular (PWMH)
white matter hyperintensities, were segmented and
characterized in terms of their quantitative properties. The
subjects were then further divided into four grades
according to the Fazekas rating scale of severity. Groupwise
analyses of the qMRI values in each tissue class were
performed. All five qMRI parameters showed significant
differences between WMH and NAWM (p < 0.001).
Importantly, the parameters differed between DWMH and PWMH,
the latter having higher H2O, T1, T2∗ and lower MTR and
ƒbound values (p < 0.001). Following grading according
to the Fazekas scale, DWMH showed an increase in the water
content, T1 and a decrease in bound proton fraction
corresponding to severity, exhibiting significant changes in
grade 3 (p < 0.001), while NAWM revealed significantly
higher H2O values in grade 3 compared to grade 0
(p < 0.001). PWMH demonstrated an increase in T2∗
values (significant in grade 3, P < 0.001). These
results are in agreement with previous histopathological
studies and support the interpretation that both edema and
myelin loss due to a possible breakdown of the blood-brain
barrier and inflammation are the major pathological
substrates turning white matter into DWMH. Edema being an
earlier contributing factor to the pathology, as expressed
in the elevated water content values in NAWM with increasing
severity. In the case of PWMH, an altered fluid dynamic and
cerebrospinal fluid leakage exacerbate the changes. It was
also found that the pathology, as monitored by qMRI, evolves
faster in DWMH than in the PWMH following the severity.},
cin = {INM-11 / INM-4 / JARA-BRAIN},
ddc = {610},
cid = {I:(DE-Juel1)INM-11-20170113 / I:(DE-Juel1)INM-4-20090406 /
$I:(DE-82)080010_20140620$},
pnm = {573 - Neuroimaging (POF3-573)},
pid = {G:(DE-HGF)POF3-573},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31398433},
UT = {WOS:000491861000081},
doi = {10.1016/j.neuroimage.2019.116077},
url = {https://juser.fz-juelich.de/record/864417},
}