Lewy body dementia encompasses both dementia with Lewy bodies and Parkinson’s disease dementia. Although both are common causes of dementia, they remain relatively understudied. The review summarises the clinico-pathologic characteristics of Lewy Body dementia and discusses the genetic and environmental evidence contributing to the risk of developing the condition. Considering that the pathophysiology of Lewy body dementia is not yet fully understood, here we focus on the role of epigenetic mechanisms as potential key mediators of gene–environment interactions in the development of the disease. We examine available important data on genomics, epigenomics, gene expression and proteomic studies in Lewy body dementia on human post-mortem brain and peripheral tissues. Genetic variation and epigenetic modifications in key genes involved in the disorder, such as apolipoprotein E (APOE), α-synuclein (SNCA) and glucocerobrosidase (GBA), suggest a central involvement of epigenetics in DLB but conclusive evidence is scarce. This is due to limitations of existing literature, such as small sample sizes, lack of replication and lack of studies interrogating cell-type specific epigenetic modifications in the brain. Future research in the field can improve the understanding of this common but complex and rapidly progressing type of dementia and potentially open early diagnostic and effective therapeutic targets.

路易氏体痴呆包括路易氏体痴呆和帕金森氏病痴呆。尽管两者都是痴呆症的常见原因，但它们仍处于相对未被研究的状态。该综述总结了路易氏体痴呆的临床病理特征，并讨论了遗传和环境证据导致患病的风险。考虑到路易氏体痴呆症的病理生理学尚未完全了解，在此我们关注表观遗传机制在疾病发展中作为基因与环境相互作用的潜在关键介质的作用。我们研究了在人类死后大脑和周围组织的路易体痴呆症的基因组学，表观基因组学，基因表达和蛋白质组学研究方面的重要数据。涉及该疾病的关键基因的遗传变异和表观遗传修饰，如载脂蛋白E（APOE），α-突触核蛋白（SNCA）和葡萄糖酸果糖苷酶（GBA）等表明表观遗传学在DLB中具有重要作用，但缺乏确凿的证据。这是由于现有文献的局限性，例如样本量小，缺乏重复性以及缺乏研究脑中细胞类型特异性表观遗传修饰的研究。该领域的未来研究可以增进对这种常见但复杂且发展迅速的痴呆类型的理解，并有可能开放早期诊断和有效治疗靶标。缺乏复制和缺乏研究来询问大脑中细胞类型特异性表观遗传修饰的研究。该领域的未来研究可以增进对这种常见但复杂且进展迅速的痴呆类型的理解，并有可能开放早期诊断和有效治疗靶标。缺乏复制和缺乏研究来询问大脑中细胞类型特异性表观遗传修饰的研究。该领域的未来研究可以增进对这种常见但复杂且发展迅速的痴呆类型的理解，并有可能开放早期诊断和有效治疗靶标。