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@ARTICLE{Schneider:282914,
author = {Schneider, Zachary and Liu, Hui and Dehestani, Mohammad and
Makarious, Mary B and Crea, Peter Wild and Bandres-Ciga,
Sara and Gasser, Thomas and Kim, Jonggeol J},
collaboration = {Program, Global Parkinson's Genetics},
title = {{A}ssessment of {SLC}25{A}46 variants in idiopathic
{P}arkinson's disease.},
journal = {Parkinsonism $\&$ related disorders},
volume = {143},
issn = {1353-8020},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {DZNE-2025-01375},
pages = {108092},
year = {2025},
abstract = {Rare damaging variants in the SLC25A46 gene were recently
reported to be associated with optic atrophy and
parkinsonism in compound heterozygous state. Here, we
comprehensively investigated the role of SLC25A46 variation
in idiopathic Parkinson's disease (PD) by leveraging whole
genome sequencing (WGS) and genotyping imputed data from the
Global Parkinson's Genetics Program (GP2) and the
Accelerating Medicines Partnership for Parkinson's disease
initiative (AMP-PD). Our analyses included genotyping
imputed data from 19,573 PD cases and 11,748 neurologically
healthy controls of European, African Admixed, African, East
Asian, Ashkenazi Jewish, Middle Eastern, Central Asian, and
Latino and Indigenous people of the Americas ancestries from
GP2. Additionally, we mined WGS data from 924 PD patients
and 229 healthy controls, as well as 3359 PD cases and 4153
neurologically healthy controls of European ancestry from
GP2 and AMP-PD, respectively. Burden analysis of rare
non-synonymous variants across case-control individuals from
WGS data did not find evidence of SLC25A46 association with
PD. Of the four SLC25A46 variants observed, the p.K256R
variant previously reported by Bitetto et al. was found in
1/3359 controls and 1/4153 cases of European ancestry but
its association was not significant. In addition, we
identified p.E79K/p.V211M in 1/3359 controls and 1/4153
cases, without confirmation of a putative compound
heterozygosity effect due to the lack of phasing data. This
variant was also identified in Admixed American/Latin
American, African Admixed, Ashkenazi Jewish, and Central
Asian ancestries. However, no significant enrichment in
cases versus controls was observed. Our results do not
support a major role for SLC25A46 in idiopathic PD in the
European population or other ancestries, though our
imputation results require cautious interpretation for
ultra-rare variants.},
keywords = {Genetics (Other) / Parkinson's disease (Other) / Risk
factor (Other) / SLC25A46 (Other)},
cin = {AG Gasser},
ddc = {610},
cid = {I:(DE-2719)1210000},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41385895},
doi = {10.1016/j.parkreldis.2025.108092},
url = {https://pub.dzne.de/record/282914},
}