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We aimed to do a systematic review of all genetic association studies that investigated people with LBD for improving our understanding of LBD molecular genetics and for facilitating discovery of novel biomarkers and therapeutic targets for LBD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We systematically reviewed five online databases (PROSPERO protocol: CRD42018087114) and completed the quality assessment using the quality of genetic association studies tool.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Eight thousand five hundred twenty\u2010one articles were screened, and 75 articles were eligible to be included. Genetic associations of LBD with <jats:italic>APOE<\/jats:italic>, <jats:italic>GBA<\/jats:italic>, and <jats:italic>SNCA<\/jats:italic> variants have been replicated by two or more good quality studies. Our meta\u2010analyses confirmed that <jats:italic>APOE<\/jats:italic>\u2010\u03b54 is significantly associated with dementia with Lewy bodies (pooled odds ratio [POR] = 2.70; 95% CI, 2.37\u20103.07; <jats:italic>P<\/jats:italic>\u2009&lt;\u2009.001) and Parkinson's disease dementia (POR = 1.60; 95% CI, 1.21\u20102.11; <jats:italic>P<\/jats:italic> = .001). Other reported genetic associations that need further replication include variants in <jats:italic>A2M<\/jats:italic>, <jats:italic>BCHE\u2010K<\/jats:italic>, <jats:italic>BCL7C<\/jats:italic>, <jats:italic>CHRFAM7A<\/jats:italic>, <jats:italic>CNTN1<\/jats:italic>, <jats:italic>ESR1<\/jats:italic>, <jats:italic>GABRB3<\/jats:italic>, <jats:italic>MAPT<\/jats:italic>, mitochondrial DNA (mtDNA) haplogroup H, <jats:italic>NOS2A<\/jats:italic>, <jats:italic>PSEN1<\/jats:italic>, <jats:italic>SCARB2<\/jats:italic>, <jats:italic>TFAM<\/jats:italic>, <jats:italic>TREM2<\/jats:italic>, and <jats:italic>UCHL1<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The reported genetic associations and their potential interactions indicate the importance of \u03b1\u2010synuclein, amyloid, and tau pathology, autophagy lysosomal pathway, ubiquitin proteasome system, oxidative stress, and mitochondrial dysfunction in LBD. There is a need for larger genome\u2010wide association study (GWAS) for identifying more LBD\u2010associated genes. Future hypothesis\u2010driven studies should aim to replicate reported genetic associations of LBD and to explore their functional implications.<\/jats:p><\/jats:sec>","DOI":"10.1002\/gps.5260","type":"journal-article","created":{"date-parts":[[2020,1,3]],"date-time":"2020-01-03T03:39:27Z","timestamp":1578022767000},"page":"436-448","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Systematic review of genetic association studies in people with Lewy body dementia"],"prefix":"10.1002","volume":"35","author":[{"given":"Hazel","family":"Sanghvi","sequence":"first","affiliation":[{"name":"GKT School of Medical Education King's College London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ricky","family":"Singh","sequence":"additional","affiliation":[{"name":"GKT School of Medical Education King's College London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamilton","family":"Morrin","sequence":"additional","affiliation":[{"name":"GKT School of Medical Education King's College London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3203-6326","authenticated-orcid":false,"given":"Anto P.","family":"Rajkumar","sequence":"additional","affiliation":[{"name":"Department of Old Age Psychiatry, Institute of Psychiatry, Psychology &amp; Neuroscience King's College London  London UK"},{"name":"Institute of Mental Health, Division of Psychiatry and Applied Psychology University of Nottingham  Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,1,16]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000004058"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(15)00462-6"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1159\/000358051"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jagp.2012.08.014"},{"key":"e_1_2_8_6_1","doi-asserted-by":"crossref","unstructured":"MuellerC BallardC CorbettA AarslandD.The prognosis of dementia with Lewy bodies.162017:390\u2010398.","DOI":"10.1016\/S1474-4422(17)30074-1"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1097\/00019442-200403000-00009"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneurol.2010.319"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2011.10.014"},{"issue":"1","key":"e_1_2_8_10_1","first-page":"110","article-title":"Genetic factors associated with dementia in Parkinson's disease (PD)","volume":"151","author":"Romo\u2010Guti\u00e9rrez D","year":"2015","journal-title":"Gac Med Mex"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2013.1925"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(17)30400-3"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2019.04.004"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12863-015-0211-2"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1136\/bmjopen-2015-010403"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijsu.2010.02.007"},{"issue":"6","key":"e_1_2_8_17_1","first-page":"1472","article-title":"Influence of apolipoprotein E genotype on senile dementia of the Alzheimer and Lewy body types. 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