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\section{The era of the genome-wide association study}  The completion of the Human Geneome Project in 2003 ushered in a new era of genomics, and with it the prospect that heritable risk factors for complex human diseases could finally be identified. The launch of the International HapMap Project in 2003 was a further significant step towards this goal [http://hapmap.ncbi.nlm.nih.gov] \cite{20811451}. Whilst The Human Genome Project produced the first 'reference' genome, the HapMap Project focused on determining the variability between individuels and ethnic groups, by genotyping single nucleotide polymorphisms (SNPs) throughout hundreds of human genomes. Upon it's completion in 2005 the project had genotyped 1.6 millions SNPs in 1184 invididuels from 11 different ethnic populations. For the first time it was possible to understand the correlation between SNPs - linkage disequalibrium (LD) - in different ethnic populations. Providers of commercial microarrays (Illiumina and Affymetrix) harnessed knowledge of LD throughout the human genome to select a set of non-redundant SNPs that capture the genetic variability across the human genome.The era of the GWAS had arrived.  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.  \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 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 GWAS is the most recent, and included 74,046 samples genotypes at over 7 million SNPs. In the space of only five years GWAS has given the field twenty new genetic loci. However, the true success of GWAS will be judged by how these genetic clues can be harnessed.