{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T14:01:27Z","timestamp":1776088887586,"version":"3.50.1"},"reference-count":50,"publisher":"MDPI AG","issue":"4","license":[{"start":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T00:00:00Z","timestamp":1776038400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes"],"abstract":"<jats:p>Background: Parkinson\u2019s disease (PD) is clinically heterogeneous, yet the genetic architecture underlying this heterogeneity remains incompletely understood. We examined the genetic correlates of four complementary PD subtyping frameworks: the clinical motor subtype (tremor-dominant [TD] vs. postural instability\/gait difficulty [PIGD]), alpha-synuclein seed amplification assay status (SAA+ vs. SAA\u2212), the pathological subtype (brain-first vs. body-first, based on the presence of REM sleep behavior disorder), and the data-driven subtype (diffuse malignant [DM] vs. mild-motor predominant [MMP] vs. intermediate [IM]). Methods: We analyzed 1390 PD patients from the Parkinson\u2019s Progression Markers Initiative (PPMI) with genotypes available for seven PD-associated genes (LRRK2, GBA1, SNCA, PRKN, PINK1, PARK7, VPS35), including specific variant resolutions (LRRK2 G2019S, R1441G\/C\/H; GBA1 N409S, severe variants; SNCAA53T), and APOE (\u03b52\/\u03b53\/\u03b54 alleles). Genetic variant frequencies were compared across subtypes using chi-square or Fisher\u2019s exact tests with the Benjamini\u2013Hochberg false discovery rate (FDR) correction. Effect sizes were quantified using Cram\u00e9r\u2019s V. multivariable logistic regression estimated adjusted odds ratios with Wald-based 95% confidence intervals. Results: Among genotyped PD patients, LRRK2 carriers constituted 13.7% (190\/1390; 170 G2019S, 18 R1441G\/C\/H), GBA1 8.6% (119\/1390; 96 N409S, 23 severe), and SNCA 2.0% (28\/1390; all A53T). APOE \u03b54 carriers comprised 23.4% (323\/1380). SAA-negative patients were markedly enriched for LRRK2 variants (37.1% vs. 10.2%, p = 3.7 \u00d7 10\u221219, q &lt; 0.001, V = 0.25), specifically G2019S (28.5% vs. 9.6%, p = 4.9 \u00d7 10\u221211, q &lt; 0.001) and R1441G\/C\/H (7.9% vs. 0.5%, p = 2.7 \u00d7 10\u221212, q &lt; 0.001). Body-first PD was enriched for GBA1 carriers (12.3% vs. 6.7%, p = 0.004, q = 0.021) and had less LRRK2 carriers (7.9% vs. 15.0%, p = 0.002, q = 0.013). The DM subtype had the highest GBA1 frequency (14.0% vs. MMP 5.9%, p &lt; 0.001, q = 0.003). After FDR correction, 10 out of 48 univariate tests remained significant. Clinical subtypes (TD vs. PIGD) showed only nominal LRRK2 differences that did not survive FDR correction. The APOE genotype did not differ across any framework. Conclusions: PD subtypes defined by alpha-synuclein pathology (SAA), pathological onset pattern (brain-first\/body-first), and data-driven classification (DM\/MMP\/IM) show distinct genetic profiles that survive multiple comparison correction. LRRK2 variants strongly associate with SAA negativity (V = 0.25); GBA1 variants associate with the severe body-first onset and the diffuse malignant subtype.<\/jats:p>","DOI":"10.3390\/genes17040449","type":"journal-article","created":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T13:12:26Z","timestamp":1776085946000},"page":"449","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genetic Associations of Parkinson\u2019s Disease Clinical, Pathological, and Data-Driven Subtypes"],"prefix":"10.3390","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5363-6369","authenticated-orcid":false,"given":"Ahmed","family":"Negida","sequence":"first","affiliation":[{"name":"Neurology Department, Virginia Commonwealth University, Richmond, VA 23298, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0511-2429","authenticated-orcid":false,"given":"Moaz Elsayed","family":"Abouelmagd","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, Cairo University, Cairo 11956, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-8049-5209","authenticated-orcid":false,"given":"Belal Mohamed","family":"Hamed","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, Al-Azhar University, Cairo 11884, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0361-4609","authenticated-orcid":false,"given":"Yousef","family":"Hawas","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, Tanta University, Tanta 31527, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aya","family":"Dziri","sequence":"additional","affiliation":[{"name":"Faculty of General Medicine, Dnipro State Medical University, 49044 Dnipro, Ukraine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-4018-8146","authenticated-orcid":false,"given":"Yasmin","family":"Negida","sequence":"additional","affiliation":[{"name":"Neurology Department, Virginia Commonwealth University, Richmond, VA 23298, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0602-9942","authenticated-orcid":false,"given":"Brian D.","family":"Berman","sequence":"additional","affiliation":[{"name":"Neurology Department, Virginia Commonwealth University, Richmond, VA 23298, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew J.","family":"Barrett","sequence":"additional","affiliation":[{"name":"Neurology Department, Virginia Commonwealth University, Richmond, VA 23298, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2026,4,13]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"525","DOI":"10.1016\/S1474-4422(06)70471-9","article-title":"Epidemiology of Parkinson\u2019s disease","volume":"5","author":"Breteler","year":"2006","journal-title":"Lancet Neurol."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"106000","DOI":"10.1016\/j.parkreldis.2024.106000","article-title":"Update: Descriptive epidemiology of Parkinson disease","volume":"120","author":"Grotewold","year":"2024","journal-title":"Park. 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