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\usepackage{pdflscape}  \section{Introduction}  Alzheimer's disease (AD) is an incurable neurodegenerative disease and the most common form of dementia, affecting approximately 850,000 people in the United Kingdom (Alzheimer's Society 2014. Dementia 2014: An opportunity for change). AD typically manifests as insidious cognitive decline with episodic memory loss and, neuropathologically, as gross cortical atrophy of the temporal cortex. Neuronal neurofibrillary tangles of hyperphosphorylated tau protein and extracellular plaques of the amyloid$\beta$ peptide are classic hallmark of AD, and provide conclusive difinative  evidence of LOAD post-mortem. Familial forms of AD are rare; manifesting early (early-onset Alzheimer's disease or EOAD) they are the result of highly penetrant, autosomal dominant mutations within genes on the 'amyloid' pathway (\textit{APP}, \textit{PSEN1} and \textit{PSEN2}). However, approximately 95 percent of AD cases are of late onset (late onset Alzheimer's disease or LOAD). Typically presenting after the fifth decade, LOAD is aetiologically highly complex, involving multiple genetic and environmental risk factors. Although not a familial disease, it has been approximated that upwards of 60 percent of LOAD liability is genetic.