Duarte-Zambrano Felipe, Alfonso-Cedeño David Felipe, Barrero Jorge A, Rodríguez-Vanegas Luis Alejandro, Moreno-Cárdenas Valentina, Olarte-Díaz Anamaría, Arboleda Gonzalo, Arboleda Humberto
Semillero de Investigación en Neurociencias, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá, Colombia.
Grupo de Investigación en Neurociencias y Muerte Celular, Facultad de Medicina E Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia.
Neurogenetics. 2025 Apr 3;26(1):43. doi: 10.1007/s10048-025-00817-8.
Idiopathic Parkinson's disease (PD) constitutes a complex trait influenced by genetic, environmental, and lifestyle factors, with an estimated heritability of nearly 30%. However, a large proportion of the heritable variation linked to PD remains uncertain, partly due to ancestral bias. Expanding research into Hispanic populations can contribute to address this gap. To review the evidence of genetic variants associated with idiopathic PD in Latin America. A PRISMA-compliant systematic review was conducted in MEDLINE, EMBASE and LILACS, compiling studies published up to February 7, 2025. Nineteen case-control studies were included. Two hypothesis-free studies identified rs525496 near H2BW1 as a protective factor and rs356182 in SNCA as a risk factor through XWAS and GWAS, respectively. Seventeen hypothesis-driven studies examined over three hundred variants, identifying nineteen genetic markers; risk factors included one INDEL in NR4A2, CNV burdens in PRKN, SNCA, and PLA2G6, along with fourteen variants in six loci including GBA, APOEε4, MTHFR, LRRK2, and SNCA. Three SNPs in the PICALM, ALDH1A1, and APOE-ε3 loci were identified as protective factors. Additionally, six SNCA variant haplotypes appear to increase PD risk, while two NR4A2 INDELs haplotypes showed mixed effects. This review summarized genetic loci associated with idiopathic PD in Latin American populations evidencing an overlap with European findings as well as novel loci, although awaiting replication and validation. These observations contribute to the understanding of genetic configuration of the disease and highlight the need for further genomic research in underrepresented groups that include local ancestry analysis within admixed cohorts to guide development of personalized treatments and population-specific interventions.
特发性帕金森病(PD)是一种受遗传、环境和生活方式因素影响的复杂性状,估计遗传度近30%。然而,与PD相关的很大一部分遗传变异仍不确定,部分原因是存在祖先偏差。扩大对西班牙裔人群的研究有助于填补这一空白。为了综述拉丁美洲与特发性PD相关的基因变异证据。我们在MEDLINE、EMBASE和LILACS上进行了一项符合PRISMA标准的系统综述,收集截至2025年2月7日发表的研究。纳入了19项病例对照研究。两项无假设研究分别通过全基因组外显子组关联研究(XWAS)和全基因组关联研究(GWAS)确定H2BW1附近的rs525496为保护因素,而突触核蛋白(SNCA)中的rs356182为风险因素。17项有假设驱动的研究检测了三百多个变异,确定了19个遗传标记;风险因素包括核受体亚家族4A组成员2(NR4A2)中的一个插入缺失(INDEL)、帕金森蛋白(PRKN)、突触核蛋白(SNCA)和磷脂酶A2G6(PLA2G6)中的拷贝数变异负担,以及包括葡萄糖脑苷脂酶(GBA)、载脂蛋白Eε4(APOEε4)、亚甲基四氢叶酸还原酶(MTHFR)、富亮氨酸重复激酶2(LRRK2)和突触核蛋白(SNCA)在内的六个基因座中的14个变异。磷脂酰肌醇结合网格蛋白组装蛋白(PICALM)、醛脱氢酶1A1(ALDH1A1)和载脂蛋白Eε3(APOE-ε3)基因座中的三个单核苷酸多态性(SNP)被确定为保护因素。此外,六个突触核蛋白(SNCA)变异单倍型似乎会增加PD风险,而两个核受体亚家族4A组成员2(NR4A2)插入缺失单倍型显示出混合效应。本综述总结了拉丁美洲人群中与特发性PD相关的基因座,证明与欧洲的研究结果有重叠,也有新的基因座,尽管尚待重复验证。这些观察结果有助于理解该疾病的遗传结构,并强调需要在代表性不足的群体中开展进一步的基因组研究,包括在混合队列中进行本地血统分析,以指导个性化治疗和针对特定人群的干预措施的开发。