transmitted diseases should be concordant in monozygotic twins, this does not appear to be the case in AD. For instance both Creasey et al. (1989) and Kumar et al. (1991) have reported three pairs of monozygotic twins who were discordant. Whereas Nee et al. (1987) only found a 41% concordance rate for AD in 17 monozygotic twins.Farrer et al. (1990) suggest that AD appears as an autosomal dominant in families in which the average age of onset among kindreds is under 58. Supporting evidence for this comes from studies which have linked EOAD with DS (Lezak, 1993). Individuals who are afflicted with Down syndrome and who survive to age 40 almost invariably develop Alzheimer like dementia. During the intermediate and terminal stages of DS the individual suffers from recent memory loss, apraxia, temporal disorientation, and mutism, all of which are also common in AD (Morris, 1994). Thus it is not surprising that four studies have found an increased risk for AD with late maternal age (Morris, 1994). The increased risk of AD to patients born to mothers over 40 is consistent with Down syndrome risk curve (Rocca et al. , 1991).Both EOAD and DS have been localized to chromosome 21. However, chromosome 21 does not appear to be a very good genetic marker for EOAD (Green book, 104). Recent studies have shown that a defect in chromosome 14 is more likely to be associated with EOAD, but the specific gene(s) have not yet been isolated (Green book, 104). Evidence for genetic predisposition to LOAD has only emerged over the last two years. It is now known that a gene which codes for a lipoprotein called ApolipoproteinE (APOE) in chromosome 19 is involved (Green book, 101). APOE is linked to the type 4 allele (e4). It has now been proven that an increase risk for dementia is dependent on a strong chemical binding between the main ingredient of SP, the Beta amyloid protein, and the APOE-e4 (Green book, 102). Table 2 summarizes the genetic fin...
