Impact of <scp><i>APOE</i></scp> Genotype on Cognition in Idiopathic and Genetic Forms of Parkinson's Disease
Christos Koros, Kathrin Brockmann, Athina‐Maria Simitsi, Anastasia Bougea, Hui Liu, Ann‐Kathrin Hauser, Claudia Schulte, Stefanie Lerche, Ioanna Pachi, Nikolaos Papagiannakis, Roubina Antonelou, Athina Zahou, Isabel Wurster, Efthymia Efthymiopoulou, Ion Beratis, Matina Maniati, Marina Moraitou, Helen Michelakakis, Georgios Paraskevas, Sokratis G. Papageorgiou, Constantin Potagas, Dimitra Papadimitriou, Maria Bozi, María Stamelou, Thomas Gasser, Leonidas Stefanis
Abstract
The data supporting the findings of this study are available upon reasonable request from any qualified investigator. Data S1. Supporting Information. Figure S1. The frequency of presence of at least one APOE ε4 allele (either in heterozygous or in homozygous form) in the idiopathic PD subgroup and in the genetic subgroups (p.A53T SNCA PD and GBA1 PD). Figure S2. MoCA scores in APOE ε4 carriers and non-carriers of the idiopathic PD subgroup (Fig. 2A). MoCA scores in APOE ε4 carriers and non-carriers of the p.A53T SNCA PD subgroup (Fig. 2B). Figure S3. MoCA scores in APOE ε4 carriers and non-carriers of the Athens GBA1 PD subgroup (Fig. 3A). MoCA scores in APOE ε4 carriers and non-carriers of the Tubingen GBA1 PD subgroup (Fig. 3B). Table S2. Demographic, clinical, and CSF biomarker in PDGBA (first visit with biomarker). Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.