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More recently the 1000 Genomes Project (1KP) has provided a much finer map of human genetic variation. The combination of genome (7.4x) and deep exome (65.7x) sequencing in over 2500 samples has enabled a more comprehensive catalouge of over 88 million variant sites to be discovered, including rare and structural changes. This has has several important applications, including designing arrays of rarer coding changes ('exome chips') and as a database to exclude pathogenic variants. However, it is the ability impute GWAS datasets with a larger set of variants using 1KP reference hapolotypes that has been a game change \cite{26432245} .   The seminal GWAS was published in 2007 by the Wellcome Trust Case Controlm Consortium (WTCCC) \cite{17554300}. With a series of 3,000 healthy controls and 14,000 combined cases across seven common human disease, the consortium identified 24 novel genetic associations with diabetes (types I & II), coronary artery disease, Crohn's disease, rheumatoid arthritis and bipolar disorder. In order to obtain a sufficiently large case-control series for GWAS, previously independent genetic genetic began to form large consortia and user there combined resources to unearth genetic risk factors for complex human diseases. The era of the GWAS had arrived. According to the NHGRI-EBI GWAS catalogue, as of November 2015 there have been 2312 published GWAS \cite{24316577}  \section{2009: The rebirth of Alzheimer's disease genetics}  Early attempts to perform a GWAS in late-onset AD suffered from small sample numbers. As a result the early GWAS were insufficiently powered to detect any genetic risk factors other than the strong APOE association. However, in 2009, each armed with a case-control cohort of greater than 5,000 samples, two European consortia published three new genes in LOAD; \textit{CLU}, \textit{PICALM} and \textit{CR1} \cite{19734902}\cite{19734903}. This was swiftly followed by a fourth US led effort, \textit{BIN1}, in 2010 \cite{20460622}. Data pooling and meta-analysis between the US (ADGC) and European groups (GERAD) resulted in the discovery of a further five genes; \textit{ABCA7}, \textit{EPHA1}, \textit{MS4A} locus, \textit{CD2AP}, \textit{CD33} \cite{21460840} \cite{21460841}. The final traunch of genes came in 2013 as a result of international collaboration under the IGAP (International Genomics of Alzheimer's Disease Project) consortia; \textit{PTK2$\beta$}, \textit{SORL1}, \textit{HLA-DRB5/1}, \textit{SLC24A4}, \textit{CASS4}, \textit{CELF1}, \textit{ZCWPW1}, \textit{INPP5D}, \textit{MEF2C}, \textit{NME8} and \textit{FERMT2} \cite{24162737}. This was the largest LOAD GWAS to date (n=74,046) and, due to genotype imputation with 1000 Genomes Project reference haplotypes, testes over 7 million genetic variants genome-wide.