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The completion of the Human Geneome Project in 2003 ushered in a new era of genomics, and with it the expection that complex genetic diseases could now be tackled. Armed with a complete 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.   \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 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, BIN1, in 2010 \cite{20460622}. Data pooling and meta-analysis between the US (ADGC) and European groups (GERAD) resulted in a further five genes; ABCA7, EPHA1, MS4A locus, CD2AP, CD33 \cite{21460840} \cite{21460841}.