Although AD is the most frequent cause of dementia in affluent societies, vascular dementia and Lewy body dementia are also common in the elderly. Thus, many patients with AD have these comorbid diagnoses. In fact, although Lewy body dementia may occur in pure form, most patients also qualify clinically and neuropathologically for AD. The McKeith criteria for the diagnosis of Lewy body dementia include progressive dementia with coincident parkinsonism, neuroleptic sensitivity, fluctuations in cognition, and spontaneous (not drug-induced) visual hallucinations (McKeith, Galasko, Kosaka, Perry, Dickson, et al., 1996; McKeith, Perry, & Perry, 1999). If indicated, patients may be given a combined diagnosis of AD and Lewy body dementia. This combination is also termed the Lewy body variant of AD.
The Hachinski Ischemic Score (HIS; Hachinski, Lassen, & Marshall, 1974) as modified by Rosen, Terry, Fuld, Katzman, and Peck (1980) is an autopsy-validated index for the diagnosis of vascular dementia. This scale includes a history of sudden onset, stepwise progression, stroke risk factors, stroke or transient ischemic attack, asymmetry or focal signs on examination, and so on. Again, patients may have a combined diagnosis of AD and vascular dementia. Finally, other potentially confounding diagnoses are the frontotemporal dementias linked to neurofibrillary tangles (the tauopathies). Phosphorylated tau is the major component of neurofibrillary tangles, and some familial frontotemporal dementias are linked to mutations and polymorphisms in the tau gene on chromosome 17. Frontotempo-ral dementia may be distinguishable from AD by consensus criteria (Neary, Snowden, Gustafson, Passant, Stuss, et al., 1998) such as early loss of personal and social awareness, hyperorality, stereotyped perseverative behavior, and impaired word fluency and executive functions. These criteria, however, are unvalidated. Patients with frontotemporal dementia may present with marked personality changes such as impulsivity, distractibil-ity, perseveration, and disinhibition. The tauopathies include frontotempo-ral dementia plus parkinsonism, corticobasal degeneration, progressive supranuclear palsy, and Pick's disease spectrum including primary progressive aphasia. Although these disorders present very differently in early clinical stages, they may be difficult to distinguish from AD in late and vegetative stages.
For unclear reasons, the risk of developing AD is higher in Black and Hispanic compared to White populations. Although the influence of the ApoE4 polymorphism on increased AD risk is apparent in Blacks, it appears to be less potent compared to Whites. Interestingly, although Black populations in Africa and the United States have similar ApoeE4 allele frequencies, the risk of AD is much higher in the age-matched U.S. Black population. This suggests that unknown environmental factors such as diet or resultant comorbidities may be important culprits. Until recently, vascular dementia was the leading cause of dementia in Japan, but this is shifting to AD, despite a low ApoE4 allele frequency, as life expectancy increases and stroke risk factors such as hypertension are better managed.
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