Alzheimer's disease (AD) is the most common cause of dementia and characterized clinically by progressive cognitive deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioural changes. The most striking early symptom is memory loss (amnesia), which usually becomes steadily more pronounced with illness progression, with relative preservation of older memories. The pathological process consists principally of neuronal cell loss (atrophy), together with deposition of amyloid plaques and neurofibrillary tangles. Genetic factors are known to be important, and polymorphisms in three different autosomal dominant genes - Presenilin 1 (PSEN1), Presenilin 2 (PSEN2) and Amyloid Precursor Protein (APP) - have been identified that account for a small number (~5%) of cases of early-onset AD. However, for late onset AD (LOAD), only one susceptibility gene has so far been identified - the epsilon 4 allele of the APOE gene. The many non-Mendelian features of this disease (e.g. late onset, discordant twins, sex specific effects etc..) point to possible epigenetic factors that may substantially participate in the occurrence of AD. Typically, in AD brains, the neurotransmitters serotonin, acetylcholine, norepinephrine, and somatostatin are at decreased levels. In contrast, glutamate levels are usually elevated.
