ABSTRACT

Alzheimer’s disease (AD) is the most common cause of dementia. It is characterized by a progressive loss of higher cognitive functions. The strongest risk factor for sporadic AD is old age, which also coincides with the increased occurrence of cerebrovascular lesions (Table 1). Additional risk factors associated with AD vascular alterations include some forms of heart disease, atherosclerosis, high plasma cholesterol, increased fat intake, history of hypertension, diabetes mellitus, head injury, stroke, systemic inflammation and ApoE e4 (1,2). The ApoE genotype is the prime susceptibility factor for sporadic AD (3). The ApoE genotype has been linked to an increased risk and reduced age of onset of AD. The ApoE has also been associated with VaD, mild cognitive impairment (MCI) (4), impaired recovery after brain trauma, amyotrophic lateral sclerosis and Pick’s disease and, more recently, also with the risk and age of onset of Parkinson’s disease (5). The ApoE4 was found to interfere with cognitive functions in non-diseased

adult men carrying ApoE4 in comparison with non-carriers (6,7). Memory deteriorates in ApoE4 carriers before the symptomatic occurrence of MCI, prior to age 60 (8). It remains to be clarified how ApoE4 affects cognitive functioning and neurodegenerative processes. Nevertheless, the ApoE genotype may be a leading aspect in the modification process of cerebrovascular functions during ageing and the increase of the predisposition to the pathogenesis of AD (9).