2 to 4 4 higher risk) or two (5 1 to 17 9 higher risk) copies of

2 to 4.4 higher risk) or two (5.1 to 17.9 higher risk) copies of the Wortmannin order APOE-4 allele on chromosome 19. APOE-4 is a risk factor only, its presence is neither

necessary nor sufficient for the development of AD. A recent meta-analysis of more than 14 000 patients with AD and controls showed that the APOE-4 allele represents a major risk factor for AD in both men and women from Inhibitors,research,lifescience,medical a large number of racial and ethnic groups across all ages between 40 and 90 years. The genetic risk of AD attributable to APOE-4 is estimated at 45% to 60%. It appears that APOE-4 does not act by increasing Aβ production, but by enhancing Aβ aggregation or decreasing its clearance. Another recently identified putative risk factor is lipoprotein(a), which appears to protect against late-onset AD in noncarriers Inhibitors,research,lifescience,medical and is an

additional risk factor for late-onset AD in carriers of the APOE-4 allele.6 A series of retrospective studies – part of the EURODBM (European Studies of Dementia) projects – showed that, compared with men, women had an increased risk for AD, while having equal risk for vascular dementia. Women appear to be at higher risk for developing AD, only in part Inhibitors,research,lifescience,medical due to increased longevity. Because women with AD live longer than men with the disease, there are twice as many women as men in the population with this disorder. These studies also showed that low education level significantly increased the risk of AD, while family history of dementia and history of head trauma with unconsciousness Inhibitors,research,lifescience,medical did not.7,8 At the present time, the only well-established risk factors for AD are age and APOE-4. Despite this knowledge, at present, genotyping is not recommended in asymptomatic individuals, with or without a history of AD, because of the uncertain predictive value, lack of treatment to stop progression of the illness, and potential discrimination.9,10 Epidemiology AD can be divided into a familial type and a sporadic

type, Inhibitors,research,lifescience,medical and also into an early-onset type (younger than 65) and a late-onset type (older than 65). The 6-month prevalence of AD in the general population appears to be 5.5% to 9%.11 There prevalence of the disease doubles every 10 years. AD currently afflicts nearly half of the people aged 85 years and older. Individuals with cognitive deficit that do not meet the generally accepted clinical criteria for AD, but have a noticeable aminophylline decrease from prior levels of cognitive performance with problems in new learning, may have mild cognitive impairment. Recent studies show that 40% of these individuals will develop AD within 3 years. Early recognition of AD is important for treatment with cholinesterase inhibitors, reduction in caregiver stress, community support, delay in institutionalization, planning of lifestyle, and legal issues. Treatment The goals of treatment are to achieve improvement in cognition and to minimize behavioral disturbances (depression, psychosis, agitation, and insomnia).

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