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@ARTICLE{McKay:259704,
author = {McKay, Nicole S and Gordon, Brian A and Hornbeck, Russ C
and Dincer, Aylin and Flores, Shaney and Keefe, Sarah J and
Joseph-Mathurin, Nelly and Jack, Clifford R and Koeppe,
Robert and Millar, Peter R and Ances, Beau M and Chen,
Charles D and Daniels, Alisha and Hobbs, Diana A and
Jackson, Kelley and Koudelis, Deborah and Massoumzadeh,
Parinaz and McCullough, Austin and Nickels, Michael L and
Rahmani, Farzaneh and Swisher, Laura and Wang, Qing and
Allegri, Ricardo F and Berman, Sarah B and Brickman, Adam M
and Brooks, William S and Cash, David M and Chhatwal,
Jasmeer P and Day, Gregory S and Farlow, Martin R and la
Fougère, Christian and Fox, Nick C and Fulham, Michael and
Ghetti, Bernardino and Graff-Radford, Neill and Ikeuchi,
Takeshi and Klunk, William and Lee, Jae-Hong and Levin,
Johannes and Martins, Ralph and Masters, Colin L and
McConathy, Jonathan and Mori, Hiroshi and Noble, James M and
Reischl, Gerald and Rowe, Christopher and Salloway, Stephen
and Sanchez-Valle, Raquel and Schofield, Peter R and
Shimada, Hiroyuki and Shoji, Mikio and Su, Yi and Suzuki,
Kazushi and Vöglein, Jonathan and Yakushev, Igor and
Cruchaga, Carlos and Hassenstab, Jason and Karch, Celeste
and McDade, Eric and Perrin, Richard J and Xiong, Chengjie
and Morris, John C and Bateman, Randall J and Benzinger,
Tammie L S},
collaboration = {Network, Dominantly Inherited Alzheimer},
othercontributors = {Brickman, Adam M and la Fougère, Christian},
title = {{P}ositron emission tomography and magnetic resonance
imaging methods and datasets within the {D}ominantly
{I}nherited {A}lzheimer {N}etwork ({DIAN}).},
journal = {Nature neuroscience},
volume = {26},
number = {8},
issn = {1097-6256},
address = {New York, NY},
publisher = {Nature America},
reportid = {DZNE-2023-00776},
pages = {1449 - 1460},
year = {2023},
abstract = {The Dominantly Inherited Alzheimer Network (DIAN) is an
international collaboration studying autosomal dominant
Alzheimer disease (ADAD). ADAD arises from mutations
occurring in three genes. Offspring from ADAD families have
a $50\%$ chance of inheriting their familial mutation, so
non-carrier siblings can be recruited for comparisons in
case-control studies. The age of onset in ADAD is highly
predictable within families, allowing researchers to
estimate an individual's point in the disease trajectory.
These characteristics allow candidate AD biomarker
measurements to be reliably mapped during the preclinical
phase. Although ADAD represents a small proportion of AD
cases, understanding neuroimaging-based changes that occur
during the preclinical period may provide insight into early
disease stages of 'sporadic' AD also. Additionally, this
study provides rich data for research in healthy aging
through inclusion of the non-carrier controls. Here we
introduce the neuroimaging dataset collected and describe
how this resource can be used by a range of researchers.},
keywords = {Humans / Alzheimer Disease: diagnostic imaging / Alzheimer
Disease: genetics / Positron-Emission Tomography / Magnetic
Resonance Imaging / Neuroimaging / Arthrogryposis /
Mutation: genetics / Amyloid beta-Peptides: genetics /
Amyloid beta-Peptides (NLM Chemicals)},
cin = {AG Levin / Tübingen common / Clinical Research (Munich)},
ddc = {610},
cid = {I:(DE-2719)1111016 / I:(DE-2719)6000018 /
I:(DE-2719)1111015},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
experiment = {EXP:(DE-2719)DIAN-20090101},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37429916},
pmc = {pmc:PMC10400428},
doi = {10.1038/s41593-023-01359-8},
url = {https://pub.dzne.de/record/259704},
}