Interpretation of risk loci from genome-wide association studies of Alzheimer's disease.
paper
Cited
Public
- Authors
- Andrews, Shea J; Fulton-Howard, Brian; Goate, Alison
- Year
- 2020
- Journal
- The Lancet. Neurology
- PMID
- 31986256
- DOI
- 10.1016/S1474-4422(19)30435-1
- PMCID
- PMC8176461
BACKGROUND: Alzheimer's disease is a debilitating and highly heritable neurological condition. As such, genetic studies have sought to understand the genetic architecture of Alzheimer's disease since the 1990s, with successively larger genome-wide association studies (GWAS) and meta-analyses. These studies started with a small sample size of 1086 individuals in 2007, which was able to identify only the APOE locus. In 2013, the International Genomics of Alzheimer's Project (IGAP) did a meta-analysis of all existing GWAS using data from 74β046 individuals, which stood as the largest Alzheimer's disease GWAS until 2018. This meta-analysis discovered 19 susceptibility loci for Alzheimer's disease in populations of European ancestry. RECENT DEVELOPMENTS: Three new Alzheimer's disease GWAS published in 2018 and 2019, which used larger sample sizes and proxy phenotypes from biobanks, have substantially increased the number of known susceptibility loci in Alzheimer's disease to 40. The first, an updated GWAS from IGAP, included 94β437 individuals and discovered 24 susceptibility loci. Although IGAP sought to increase sample size by recruiting additional clinical cases and controls, the two other studies used parental family history of Alzheimer's disease to define proxy cases and controls in the UK Biobank for a genome-wide association by proxy, which was meta-analysed with data from GWAS of clinical Alzheimer's disease to attain sample sizes of 388β324 and 534β403 individuals. These two studies identified 27 and 29 susceptibility loci, respectively. However, the three studies were not independent because of the large overlap in their participants, and interpretation can be challenging because different variants and genes were highlighted by each study, even in the same locus. Furthermore, neither the variant with the strongest Alzheimer's disease association nor the nearest gene are necessarily causal. This situation presents difficulties for experimental studies, drug development, and other future research. WHERE NEXT?: The ultimate goal of understanding the genetic architecture of Alzheimer's disease is to characterise novel biological pathways that underly Alzheimer's disease pathogenesis and to identify novel drug targets. GWAS have successfully contributed to the characterisation of the genetic architecture of Alzheimer's disease, with the identification of 40 susceptibility loci; however, this does not equate to the discovery of 40 Alzheimer's disease genes. To identify Alzheimer's disease genes, these loci need to be mapped to variants and genes through functional genomics studies that combine annotation of variants, gene expression, and gene-based or pathway-based analyses. Such studies are ongoing and have validated several genes at Alzheimer's disease loci, but greater sample sizes and cell-type specific data are needed to map all GWAS loci.
Combined Manhattan plot of four Alzheimerβs disease GWAS, showing loci with genome-wide significanceColoured circles represent loci that had genome-wide significance in each study, while empty circles represent non-significant loci for each study. GWAS=genome-wide association studies.
| # | Section | Preview |
|---|---|---|
| 20 | Introduction β From loci to genes | The 2019 GWAS9 identified 53 genes across 20 non-APOE loci with a priority score of greater than 5;β¦ |
| 21 | Introduction β From loci to genes | PVR and TOMM40 also have further evidence of brainβspecific eQTL and methylation QTLs (mQTLs).β¦ |
| 22 | Introduction β From loci to genes | 11 genes overlapped between the analyses in the 2019 GWAX7 and in the 2019 GWAS:9 CR1, BIN1,β¦ |
| 23 | Introduction β From loci to genes | A limitation of functional genomics studies in Alzheimerβs disease is the lack of wellβpoweredβ¦ |
| 24 | Introduction β From loci to genes | The limitations of functional genomics are high lighted in the APOE locus in which the combinationβ¦ |
| 25 | Introduction β Conclusions and future directions | GWAS have identified 40 loci that are associated with Alzheimerβs disease in European populations,β¦ |
β Prev
21β26 of 26
| Name | Type |
|---|---|
| 16p12.3 local | variant |
| 16q23.3 local | variant |
| 17q21.33 local | variant |
| 18q21.31 local | variant |
| 19p13.3 local | variant |
| 2013 GWAS local | cohort |
| 2018 GWAX local | cohort |
| 2018 GWAX7 local | cohort |
| 2019 GWAS local | cohort |
| 2019 GWAS9 local | cohort |
| 2019 GWAX local | cohort |
| 2019 GWAX7 local | cohort |
| 2019 GWAX8 local | cohort |
| 21q21.3 local | variant |
| 5q14.3 local | variant |
| 6p21.1 local | variant |
| 78 unique lead SNPs local | variant |
| 7p14.1 local | variant |
| 7q22.1 local | variant |
| 7q35 local | variant |
| ABCA7 | gene |
| Adam10 | gene |
| Alzheimer Disease Genetics Consortium local | cohort |
| Alzheimer's disease | phenotype |
| Alzheimerβs disease | phenotype |
| Alzheimerβs disease GWAS local | cohort |
| Alzheimerβs disease GWAS cohorts local | cohort |
| Alzheimerβs Disease Sequencing Project local | cohort |
| amyloid plaques | phenotype |
| amyloid Ξ² | drug |
| amyloid Ξ² peptides local | drug |
| APOC1 local | gene |
| APOC4 | gene |
| apoE | gene |
| APP | gene |
| BCAM local | gene |
| BIN1 | gene |
| brain tissue | anatomy |
| candidate causal variant local | variant |
| CASS4 local | gene |
| CD2AP local | gene |
| CD33 | gene |
| CHARGE | cohort |
| CLPTM1 local | gene |
| Clu | gene |
| cognitively normal individuals local | phenotype |
| community-based autopsy cohort local | cohort |
| CR1 | gene |
| dementia | phenotype |
| early-onset Alzheimerβs disease dementia local | phenotype |
| ethnic groups | cohort |
| European Alzheimer Disease Initiative local | cohort |
| European ancestry | cohort |
| European population | cohort |
| extracellular plaques local | phenotype |
| functional variant | variant |
| gene | gene |
| Genetic and Environmental Risk in Alzheimerβs Disease local | cohort |
| genetic variants | cohort |
| gliosis | phenotype |
| GWAS | cohort |
| GWAS9 (2019) local | cohort |
| GWAX local | cohort |
| GWAX7 local | cohort |
| GWAX7 (2019) local | cohort |
| HLA-DRB1 local | gene |
| hyperphosphorylated tau | drug |
| IGAP | cohort |
| IGAP GWAS | cohort |
| IGSF23 local | gene |
| immune response pathways local | phenotype |
| large-scale biobanks local | cohort |
| late-onset Alzheimerβs disease dementia local | phenotype |
| lead SNP | cohort |
| Lewy body pathology local | phenotype |
| lipid traits local | phenotype |
| Maternal family history of Alzheimer's disease local | phenotype |
| microglia | phenotype |
| MS4A4A local | gene |
| MS4A6A local | gene |
| neurodegeneration | phenotype |
| neurofibrillary tangles | phenotype |
| neuro inflammation local | phenotype |
| NYAP1 local | gene |
| Paternal family history of Alzheimer's disease local | phenotype |
| peripheral myeloid cells local | anatomy |
| PICALM | gene |
| PILRA local | gene |
| population stratification | phenotype |
| PSEN1 | gene |
| PSEN2 | gene |
| Psychiatric Genomics Consortium | cohort |
| PT2KB local | gene |
| PVR local | gene |
| SNP | cohort |
| SORL1 | gene |
| SPI1 | gene |
| study cohort | cohort |
| susceptibility loci local | variant |
| tau | phenotype |
| tau burden local | phenotype |
| TDP-43 pathology local | phenotype |
| TOMM40 local | gene |
| top variant local | variant |
| trait | phenotype |
| TREM2 | gene |
| UK Biobank | cohort |
| vascular disease pathology local | phenotype |
| ZCWPW1 local | gene |
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