[Truncated abstract.] Alzheimer’s disease (AD) is the most common form of dementia world-wide accounting for more than two thirds of all dementia cases. AD is characterised by the presence of extracellular amyloid plaques, neurofibrillary tangles and congophillic amyloid angiopathy in the brain tissue of affected individuals. Of these neuropathological features the extracellular amyloid plaques are the most characteristic containing a peptide termed amyloid- beta (Aβ); the major protein component of these structures. In addition a number of genetic risk factors for AD have been identified. Of these the ε4 allele of the apolipoprotein E (APOE) gene found on chromosome 19 is considered to be the main genetic risk factor attributing to about 40-60% of all AD cases in most populations. Although there is strong evidence that genetic risk factors play an important role in AD they do not actually trigger the disease process. Deficits in memory and learning are the most common clinical signs of AD in the initial stages of the disease. Neuropsychological tests such as the CAMCOG and California Verbal Learning Test (CVLT) are important diagnostic tools used for the assessment of cognition. The CAMCOG is an accurate and efficient measure of global cognitive ability, while the CVLT is more specific to areas of cognition influenced in the early stages of the disease such as verbal memory. Substantial evidence indicates that changes in sex hormones following menopause in women are important factors in AD. Specifically, the reduced levels of oestrogen in post-menopausal women have been linked to cognitive decline and an increased risk of dementia. In addition the elevated level of the gonadotropins, a characteristic of the post-menopausal period, have been implicated with the disease. Numerous nonhormonal factors such as age and education may also be associated with the development and progression of cognitive decline.