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\section{Introduction}  Alzheimer's disease (AD) is an incurable neurodegenerative disease and the most common form of dementia dementia,  affecting approximatly 750,000 people in the United Kingdom. Although the clinical manifestations of AD are striking, typically presenting as cognitive decline with progressive episodic memory loss, difinative definitive  diagnosis required requires  neuropathological examination post-mortem. Neuropathological hallamrks of AD include gross cortical atrophy, particularly of the temporal lobes and the presence of; i) nerofibrillary tangles of hyperphosphorylated tau protein and ii) extracellular deposited of amyloid plaques containing the $\alpha\beta$ peptide of the amyloid presursor protein (APP). Whilst an early-onset, mendelian form of the disease exists (Early-onset Alzheimer's disease or EOAD), typically the results of highly penetrant autosomal dominant mutations in genes on the amyloid pathway (\textit{APP}, \textit{PSEN1} and \textit{PSEN2}), the late-onset form of the disease (Late-onset Alzheimer's disease or LOAD) is more common accounting for ~95\% of AD cases. LOAD typically manifests after the sixth decade of life and in understood to be genetically complex - the result of multiple genetic and environmental risk factors. However, twin and family based studies have estimated that the genetic component is considerable, accounting for approximatly 60-80\% of the heritability of LOAD. However, unearthing the genes involved in LOAD was going to be tricky.  
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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 our understanding of heritable risk factors for  complex genetic human  diseases would could finally  be a beneficiary. The first draft of the human genome identified.  The launch of the International HapMap Project in 2003 was a further significant  step towards this goal. 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.  Armed with the human reference genome, understanding the variability between humans became a major focus of the International HapMap Project [http://hapmap.ncbi.nlm.nih.gov] \cite{20811451}. 1184 1.6 million 11 different ethnic populations. Microarray. Consortia. WTCCC. What is GWAS.  A genome-wide association study (GWAS) uses microarray technology to genotype hundreds of thousands (more recently millions) of single nucleotide polymorphisms (SNPs) from across the genome. Knowledge of linkage disequalibrium throughout the human genome allowed for intelligent selection of a non redundant set of SNPs that capture genetic variability across the human genome. The era of the GWAS had arrived. Thefirst  seminal GWAS was published in 2007 by the Wellcome Trust Case Controlm Consortium (WTCCC). (WTCCC) \cite{17554300}.  \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.