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\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.  \begin{table}   \begin{tabular}{ l || l | l | l | c }  \hline\hline 
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\begin{tabular}{ l || l | l | l | c }  \hline\hline  Gene or Locus & SNP & MAF & Genomic Location & Odds Ratio \\  \hline  \textit{CLU} & rs9331896 & 0.40 & Intronic & 0.86 (0.84-0.89) \\   \textit{PICALM} & rs10792832 & 0.37 & Intergenic & 0.87 (0.85-0.89) \\   \textit{CR1} & rs6656401 & 0.19 & Intronic & 1.18 (1.14 -1.22) \\