Alzheimer’s disease (AD) is a devastating neurologic disorder that affects more than 20 million individuals of all races and ethnic backgrounds. The incidence of AD in the general population is about 1%, with a prevalence of 5–15% in people older than 65 years of age. AD is an etiologically and genetically heterogeneous disorder. So far, 4 chromosomes have been implicated in the etiopathogenesis of AD. Several missense mutations in the amyloid precursor protein gene (APP) on chromosome 21 have been found in about 3% of familial early-onset AD. This familial pattern is consistent with an autosomal dominant inheritance (St. George-Hyslop et al., 1987). In 1992, two different groups discovered genetic linkage to a major familial AD gene defect on chromosome 14 in the region 14q24.3 (St.George-Hyslop et al., 1992; Schellenberg et al., 1992). In that region, several candidate genes have been postulated, including c-fos and presenilin 1 (Van Broeckhoven et al., 1992; Mullan et al., 1992; Sherrington et al., 1995). An intronic polimorphism located at 3’to exon 8 of the presenilin 1 (PSI) gene was described (Wragg et al., 1996). The most common allele has an adenine at nucleotide position 16 (allele 1) in the intron, while the variant allele has a cytosine at the same position (allele 2). Neither the 1/2 genotype nor the 2/2 genotype were associated with increased risk for AD, whereas the 1/1 genotype was associated with an approximately 2-fold risk.The STM2 gene maps on chromosome 1 and was also found to have two point mutations segregating in early-onset AD families (Levy-Lahad et al., 1995). In the nineties several groups showed evidence for an AD susceptibility gene on chromosome 19 (Pericak-Vance et al., 1991; Farrer et al., 1992; Stritmatter et al., 1993). The responsible gene was the APOE gene located at 19ql3.2, which encodes apolipoprotein E (ApoE), a 34 kD glycosilated protein associated with plasma lipoproteins (Weisgraber, 1994; Hallmann et al., 1991). Three common APOE variants are encoded by three APOE alleles: εl, ε;3 and ε4. Several groups have reported an association between late-onset AD or sporadic AD and the APOε4 allele (Saunders et al., 1993; Beyer et al., 1996). The risk of suffering AD-type dementia increases with the number of associated genetic factors identified in an individual. Consistent with the APOE ε4-late onset AD association, the presence of ApoE4 in the characteristic AD brain lesions, such as senile plaques, and neurofibrillary tangles has been demonstrated (Namba et al., 1991). It is known that in vitro Apo e4 binds more avidly to β-amyloid peptide (βA) than ApoE3 in order to form stable ApoE-βA complexes that would result in βA deposition (Strittmatter et al., 1993; Sanan et al., 1994). In contrast, another major protein implicated in AD, tau protein, binds strongly in vitro to ApoE3 but not to ApoE4. One hypothesis proposes that Apo E3-tau interactions serve as a protective mechanism against tau phosphorilation (Strittmatter et al., 1994). It is well known the function of ApoE in peripheral lipid metabolism and in the homeostasis of cholesterol. The role of ApoE in the brain is not well understood although it seems to be related to the redistribution of cholesterol within neuronal tissues undergoing repair or remodeling (Boyles et al., 1989). Poitier et al (1991) demonstrated that ApoE is important in the transport and redistribution of cholesterol during membrane remodelling in the central nervous system of the rat. Serum ApoE levels were measured by different groups in healthy and disease states. ApoE concentrations vary as a function of different biological factors as age, decreasing ApoE levels after the age of 60 (Siest et al., 1995). Several other groups also studied the levels of ApoE in AD patients. Lehtimäki et al. in 1995 found that ApoE concentrations in cerebrospinal fluid were lower in AD patients than in healthy subjects, but they did not find differences among ApoE phenotypes. Serum ApoE levels in AD patients could also be different from healthy subjects due to the implication of ApoE in the etiopathogenesis of AD. In this study, we measured serum ApoE, total-cholesterol, triglycerides and lipoproteins-cholesterol levels in AD patients and control subjects in order to know the influence of the APOE genotype on the serum levels of these biochemical parameters, and to assess if AD patients have a different lipid and lipoprotein profile than controls.