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@ARTICLE{Makarious:163706,
author = {Makarious, Mary B. and Leonard, Hampton L. and Vitale, Dan
and Iwaki, Hirotaka and Sargent, Lana and Dadu, Anant and
Violich, Ivo and Hutchins, Elizabeth and Saffo, David and
Bandres-Ciga, Sara and Kim, Jonggeol Jeff and Song, Yeajin
and Maleknia, Melina and Bookman, Matt and Nojopranoto,
Willy and Campbell, Roy H. and Hashemi, Sayed Hadi and
Botia, Juan A. and Carter, John F. and Craig, David W. and
Van Keuren-Jensen, Kendall and Morris, Huw R. and Hardy,
John A. and Blauwendraat, Cornelis and Singleton, Andrew B.
and Faghri, Faraz and Nalls, Mike A.},
title = {{M}ulti-modality machine learning predicting
{P}arkinson’s disease},
journal = {npj Parkinson's Disease},
volume = {8},
number = {1},
issn = {2373-8057},
address = {London [u.a.]},
publisher = {Nature Publ. Group},
reportid = {DZNE-2022-00445},
pages = {35},
year = {2022},
abstract = {Personalized medicine promises individualized disease
prediction and treatment. The convergence of machine
learning (ML) and available multimodal data is key moving
forward. We build upon previous work to deliver multimodal
predictions of Parkinson’s disease (PD) risk and
systematically develop a model using GenoML, an automated ML
package, to make improved multi-omic predictions of PD,
validated in an external cohort. We investigated top
features, constructed hypothesis-free disease-relevant
networks, and investigated drug–gene interactions. We
performed automated ML on multimodal data from the
Parkinson’s progression marker initiative (PPMI). After
selecting the best performing algorithm, all PPMI data was
used to tune the selected model. The model was validated in
the Parkinson’s Disease Biomarker Program (PDBP) dataset.
Our initial model showed an area under the curve (AUC) of
$89.72\%$ for the diagnosis of PD. The tuned model was then
tested for validation on external data (PDBP, AUC
$85.03\%).$ Optimizing thresholds for classification
increased the diagnosis prediction accuracy and other
metrics. Finally, networks were built to identify gene
communities specific to PD. Combining data modalities
outperforms the single biomarker paradigm. UPSIT and PRS
contributed most to the predictive power of the model, but
the accuracy of these are supplemented by many smaller
effect transcripts and risk SNPs. Our model is best suited
to identifying large groups of individuals to monitor within
a health registry or biobank to prioritize for further
testing. This approach allows complex predictive models to
be reproducible and accessible to the community, with the
package, code, and results publicly available.},
cin = {Tübingen common / AG Gasser},
ddc = {610},
cid = {I:(DE-2719)6000018 / I:(DE-2719)1210000},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC8975993},
pubmed = {pmid:35365675},
doi = {10.1038/s41531-022-00288-w},
url = {https://pub.dzne.de/record/163706},
}