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@ARTICLE{Preische:140473,
author = {Preische, Oliver and Schultz, Stephanie A and Apel, Anja
and Kuhle, Jens and Kaeser, Stephan A and Barro, Christian
and Gräber, Susanne and Kuder-Buletta, Elke and la
Fougère, Christian and Laske, Christoph and Vöglein,
Jonathan and Levin, Johannes and Masters, Colin L and
Martins, Ralph and Schofield, Peter R and Rossor, Martin N
and Graff-Radford, Neill R and Salloway, Stephen and Ghetti,
Bernardino and Ringman, John M and Noble, James M and
Chhatwal, Jasmeer and Goate, Alison M and Benzinger, Tammie
L S and Morris, John C and Bateman, Randall J and Wang,
Guoqiao and Fagan, Anne M and McDade, Eric M and Gordon,
Brian A and Jucker, Mathias and Network, Dominantly
Inherited Alzheimer and Allegri, Ricardo and Amtashar,
Fatima and Bateman, Randall and Benzinger, Tammie and
Berman, Sarah and Bodge, Courtney and Brandon, Susan and
Brooks, William and Buck, Jill and Buckles, Virginia and
Chea, Sochenda and Chhatwal, Jasmeer and Chrem, Patricio and
Chui, Helena and Cinco, Jake and Clifford, Jack and
Cruchaga, Carlos and D'Mello, Mirelle and Donahue, Tamara
and Douglas, Jane and Edigo, Noelia and Erekin-Taner,
Nilufer and Fagan, Anne and Farlow, Marty and Farrar, Angela
and Feldman, Howard and Flynn, Gigi and Fox, Nick and
Franklin, Erin and Fujii, Hisako and Gant, Cortaiga and
Gardener, Samantha and Ghetti, Bernardino and Goate, Alison
and Goldman, Jill and Gordon, Brian and Graff-Radford, Neill
and Gray, Julia and Gurney, Jenny and Hassenstab, Jason and
Hirohara, Mie and Holtzman, David and Hornbeck, Russ and
DiBari, Siri Houeland and Ikeuchi, Takeshi and Ikonomovic,
Snezana and Jerome, Gina and Karch, Celeste and Kasuga,
Kensaku and Kawarabayashi, Takeshi and Klunk, William and
Koeppe, Robert and Kuder-Buletta, Elke and Lee, Jae-Hong and
Marcus, Daniel and Martins, Ralph and Mason, Neal Scott and
Masters, Colin and Maue-Dreyfus, Denise and McDade, Eric and
Montoya, Lucy and Mori, Hiroshi and Morris, John and
Nagamatsu, Akem and Neimeyer, Katie and Noble, James and
Norton, Joanne and Perrin, Richard and Raichle, Marc and
Ringman, John and Roh, Jee Hoon and Salloway, Stephen and
Schofield, Peter and Shimada, Hiroyuki and Shiroto, Tomoyo
and Shoji, Mikio and Sigurdson, Wendy and Sohrabi, Hamid and
Sparks, Paige and Suzuki, Kazushi and Swisher, Laura and
Taddei, Kevin and Wang, Jen and Wang, Peter and Weiner, Mike
and Wolfsberger, Mary and Xiong, Chengjie and Xu, Xiong},
title = {{S}erum neurofilament dynamics predicts neurodegeneration
and clinical progression in presymptomatic {A}lzheimer's
disease.},
journal = {Nature medicine},
volume = {25},
number = {2},
issn = {1078-8956},
address = {New York, NY},
publisher = {Nature America Inc.},
reportid = {DZNE-2020-06795},
pages = {277-283},
year = {2019},
abstract = {Neurofilament light chain (NfL) is a promising fluid
biomarker of disease progression for various cerebral
proteopathies. Here we leverage the unique characteristics
of the Dominantly Inherited Alzheimer Network and
ultrasensitive immunoassay technology to demonstrate that
NfL levels in the cerebrospinal fluid (n = 187) and
serum (n = 405) are correlated with one another and are
elevated at the presymptomatic stages of familial
Alzheimer's disease. Longitudinal, within-person analysis of
serum NfL dynamics (n = 196) confirmed this elevation
and further revealed that the rate of change of serum NfL
could discriminate mutation carriers from non-mutation
carriers almost a decade earlier than cross-sectional
absolute NfL levels (that is, 16.2 versus 6.8 years before
the estimated symptom onset). Serum NfL rate of change
peaked in participants converting from the presymptomatic to
the symptomatic stage and was associated with cortical
thinning assessed by magnetic resonance imaging, but less so
with amyloid-β deposition or glucose metabolism (assessed
by positron emission tomography). Serum NfL was predictive
for both the rate of cortical thinning and cognitive changes
assessed by the Mini-Mental State Examination and Logical
Memory test. Thus, NfL dynamics in serum predict disease
progression and brain neurodegeneration at the early
presymptomatic stages of familial Alzheimer's disease, which
supports its potential utility as a clinically useful
biomarker.},
subtyp = {Letter},
keywords = {Alzheimer Disease: blood / Alzheimer Disease: cerebrospinal
fluid / Alzheimer Disease: pathology / Disease Progression /
Humans / Mutation: genetics / Nerve Degeneration: blood /
Neurofilament Proteins: blood / Neurofilament Proteins:
cerebrospinal fluid / Neurofilament Proteins: genetics /
Neurofilament Proteins (NLM Chemicals) / neurofilament
protein L (NLM Chemicals)},
cin = {AG Jucker / Core ICRU / Tübingen common / AG Höglinger 1
/ Clinical Research (Munich) / AG Levin},
ddc = {610},
cid = {I:(DE-2719)1210001 / I:(DE-2719)1240005 /
I:(DE-2719)6000018 / I:(DE-2719)1110002 / I:(DE-2719)1111015
/ I:(DE-2719)1111016},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
- Clinical and Health Care Research (POF3-344)},
pid = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30664784},
pmc = {pmc:PMC6367005},
doi = {10.1038/s41591-018-0304-3},
url = {https://pub.dzne.de/record/140473},
}