Relation of apolipoprotein(a) size to alzheimer's disease and vascular dementia

Lipoprotein(a) [Lp(a)] level is a newly established vascular risk factor which has been suggested to play a role in dementia. However, the majority of Lp(a) cell-to-cell interactions are mediated by its specific apolipoprotein(a) [apo(a)] moiety. This suggests that the size polymorphism of apo(a) may be of importance in conveying the Lp(a)-related risk. Specifically, we postulated that variation in apo(a) isoform size may lead to increased risk of vascular dementia (VaD), Alzheimer's disease (AD), stroke, or all three of them. Under a case-control design we compared Lp(a) plasma levels and the distribution of apo(a) phenotypes in groups of subjects consisting of 50 VaD patients, 162 sporadic AD patients, 95 non-demented stroke patients (NDS), and 105 normal controls. The prevalence of small-sized apo(a) isoforms in the VaD group was significantly higher than that in the stroke and normal control groups, with an odds ratio of 5.29 (95% CI 2.24-12.49, p = 0.0001) for the development of VaD for individuals with at least one apo(a) isoform of low molecular weight (LMW). Furthermore, the possession of at least one small-sized apo(a) isoform significantly increased the risk of AD to 1.92 (95% CI 1.02-3.61, p = 0.0434). Our results demonstrate that possession of at least one LMW apo(a) isoform is significantly associated with dementia and specifically offer new evidence of a strong association between the lipoprotein system and post-stroke dementia.     

APOE genotype, plasma lipids, lipoproteins, and AD in community elderly.

BACKGROUND: Genetic variation at the APOE locus has a major influence on both plasma lipid levels and the risk of AD. The relationship between APOE genotype and plasma lipids may influence the risk of AD. OBJECTIVE: In a community-based study of white, African American, and Caribbean Hispanic elderly in New York City, we investigated the relationship between plasma lipids and AD as well as the possible influence of APOE genotype on this relationship. METHODS: Total plasma cholesterol (TC), low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride levels were investigated in a cross-sectional study of nondemented elderly and patients with AD and in a prospective study of incident AD. Analyses included APOE genotype, gender, ethnicity, body mass index, and other potential confounders such as a history of hypertension, smoking, aspirin use, previous stroke, or ischemic heart disease. RESULTS: Compared with nondemented elderly, decreased TC level had a weak but significant inverse association with incident AD, independent of APOE genotype. No other lipoprotein fragment was associated with either prevalent or incident AD. CONCLUSION: Our results suggest that no consistent relationship exists between APOE genotype, plasma lipoproteins, and AD.     

Relation of plasma lipids to Alzheimer disease and vascular dementia

BACKGROUND: The relation between plasma lipid levels and Alzheimer disease (AD) and vascular dementia (VaD), and the impact of drugs to lower lipid levels remains unclear. OBJECTIVE: To investigate the relation between plasma lipid levels and the risk of AD and VaD and the impact of drugs to lower lipid levels on this relationship. DESIGN AND SETTING: Cross-sectional and prospective community-based cohort studies. PARTICIPANTS: Random sample of 4316 Medicare recipients, 65 years and older, residing in northern Manhattan, NY. MAIN OUTCOME MEASURES: Vascular dementia and AD according to standard criteria. RESULTS: Elevated levels of non-high-density lipoprotein (HDL-C) and low-density lipoprotein cholesterol (LDL-C) and decreased levels of HDL-C were weak risk factors for VaD in either cross-sectional or prospective analyses. Higher levels of total cholesterol were associated with a decreased risk of incident AD after adjustment for demographics, apolipoprotein E genotype, and cardiovascular risk factors. Treatment with drugs to lower lipid levels did not change the disease risk of either disorder. CONCLUSIONS: We found a weak relation between non-HDL-C, LDL-C, and HDL-C levels and the risk of VaD. Lipid levels and the use of agents to lower them do not seem to be associated with the risk of AD.     

Dual inverse effects of lipoprotein(a) on the dementia process in Japanese late-onset Alzheimer's disease

Background: The role of lipoprotein metabolism in the dementia process has attracted increasing attention. It is universally accepted that apolipoprotein E4 (ApoE) is a risk factor for late‐onset Alzheimer's disease, however, the role of lipoprotein(a) (Lp(a)) remains unclear. Therefore, we conducted the present study to clarify the association between Lp(a) and dementia. Methods: Lipoprotein(a) serum concentrations were examined in relation to ApoE phenotypes and periventricular lucency (PVL) on brain computed tomography in 150 patients with late‐onset Alzheimer's disease (AD group), compared with 46 patients with vascular dementia (VaD group) and 150 controls without dementia. Results: The incidences of hypertension, hypercholesterolaemia, and severe PVL were significantly higher in the VaD group than in the AD group. The distributions of Lp(a) concentrations showed left‐skewed deviation in each group, but we found the concentration of 40 mg/dL to be the best cut‐off point to distinguish the frequency of Alzheimer's disease from that of the controls. Compared with the frequency of high Lp(a) concentrations of 40 mg/dL or more in the controls (16.7%), that in the AD group (10.0%) was significantly lower, while that in the VaD group (45.7%) was significantly higher. Separating the AD group according to the presence or absence of ApoE4, the same findings were recognized. However, severe PVL was more frequent in the AD group with high Lp(a) concentrations (53.3%) than in the AD group without high Lp(a) concentrations (7.4%) (P < 0.01). Conclusions: These findings suggest the possibility of dual inverse effects of Lp(a) on the occurrence of Japanese late‐onset Alzheimer's disease, via suppression of Alzheimer's related processes and promotion of PVL formation presumably caused by ischemia.     

Lipoprotein(a), apolipoprotein E genotype,and risk of Alzheimer's disease

OBJECTIVES: To explore the possible role of serum lipoprotein(a) (Lp(a)), apolipoprotein E polymorphism, and total cholesterol (TC) serum concentrations in Alzheimer's disease (AD). METHODS: Lp(a) serum concentrations, apolipoprotein E genotypes, and TC serum concentrations were determined in 61 patients with a diagnosis of probable AD and in 63 healthy unrelated age matched controls. Genomic DNA was obtained and amplified by polymerase chain reaction and apolipoprotein E genotypes were defined following a previously described procedure. RESULTS: Lp(a) serum concentrations were significantly associated in a non-linear relation with an increased risk for AD, independently of apolipoprotein E genotypes and sex and dependent on age (truth association) and TC serum concentrations (spurious association). The effect of age adjusted for TC on the odds of having AD increased non-linearly with increasing Lp(a) serum concentrations, with a plateau between 70 and 355 mg/l (odds ratio 11.33). For Lp(a) serum concentrations > or = 360 mg/l, the effect of age (> or = 72 years) was associated with a reduction in odds of having AD (odds ratio 0.15). CONCLUSION: It is suggested that increased Lp(a) serum concentrations, by increasing the risk for cerebrovascular disease, may have a role in determining clinical AD.     

Serum lipoprotein profile and APOE genotype in Alzheimer's disease

Alterations in cholesterol homeostasis are associated with Alzheimer's disease (AD). The role played by specific fractions of serum lipoproteins in modifying the risk of AD, and the interaction with APOE genotype has not yet been investigated. We studied serum lipoprotein profiles using a gradient-density ultracentrifugation method in a cohort of late-onset sporadic AD patients without cerebrovascular lesions and in healthy elderly subjects. In the AD group the lipoprotein cholesterol distribution showed an increase in LDL cholesterol, reaching a significant difference with respect to controls in the LDL sub-fractions representing the transition between small dense-LDL (fraction 11, p = 0.04) and normal-density LDL particles (fraction 12, p = 0.03). APOE genotype and LDL cholesterol were independently associated with AD. The mean concentration of LDL in fractions 11 and 12 increased the risk of developing AD (p = 0.01 and p = 0.025, respectively). These results confirm that an alteration of cholesterol homeostasis is associated with AD and that serum concentrations of LDL cholesterol are higher in AD patients without cerebrovascular pathology than in elderly normal subjects. The presence of the APOE epsilon4+ allele is a risk factor for AD independent of increased serum cholesterol or a modification of other vascular risk factors. Increased levels of specific sub-fractions of LDL cholesterol may be associated with increased risk of AD.     

Elevated serum total and LDL cholesterol in very old patients with Alzheimer's disease

The relationships of serum lipids with Alzheimer's disease (AD) and other dementias in very old patients are not clear. All residents of an academic nursing home were studied clinically for dementia and for serum lipids. All those autopsied over a 7.7-year period had apolipoprotein E (apoE) genotyping and detailed neuropathological examination. Those with pathologically defined criteria for AD (n = 84) were compared to all others who also had clinical dementia but did not show AD changes (n = 22). In contrast to most other reports of serum lipids in very old patients with AD, total cholesterol (TC) and low density lipoprotein cholesterol levels were each significantly higher for those with AD. The lipid-AD associations were progressively stronger with increasing pathological certainty of AD diagnosis. These relationships remained significant after adjustment for apoE genotype and for other known risk factors. The lipid-AD associations in a very old cohort, and prior evidence that elevated TC in middle life is a risk factor for later dementia, prompt consideration of factors associated with lipid metabolism in the development of Alzheimer's dementia.     

Serum cholesterol, APOE genotype, and the risk of Alzheimer's disease: a population-based study of African Americans

A significant interaction among total serum cholesterol (TC), APOE genotype, and AD risk was found in a population-based study of elderly African Americans. Increasing TC was associated with increased AD risk in the group with no epsilon4 alleles, whereas TC was not associated with increased AD risk in the group with one or more epsilon4 alleles. Further study of the relationship between cholesterol and APOE genotype is needed to confirm this association, but the results suggest that cholesterol may be a potentially modifiable environmental risk factor for AD.     

Apolipoprotein E genotypes in hospitalized elderly patients with vascular dementia

BACKGROUND: Polymorphism in the apolipoprotein E (APOE) gene is the major genetic risk factor associated with late-onset Alzheimer's Disease (AD). However, it is still unclear if a relationship exists between the APOE epsilon4 allele and vascular dementia (VaD) in elderly subjects. OBJECTIVES: To evaluate the prevalence of APOE alleles in elderly patients with VaD compared to AD patients and to control subjects with no cognitive impairment (NoCI). PATIENTS AND METHODS: We evaluated 396 consecutive patients aged > or =65 years with definite or suspected cognitive impairment with a clinical (Mini-Mental State Examination, Clinical Dementia Rating, Geriatric Depression Scale), functional (Activities of Daily Living, Instrumental Activities of Daily Living), comorbidity (Cumulative Illness Rating Scale) and instrumental (CT scan, NMR) assessment. Diagnosis of dementia was made according to NINCDS-ADRDA and NINDS-AIREN Work Group and the DSM-IV. APOE genotypes were analyzed by a recently described method resulting in positive/negative chain reaction products for each APOE genotype. Statistical analysis was carried out using the Pearson chi(2), the Kruskal-Wallis test and the ANOVA post hoc comparisons. RESULTS: A total of 287 elderly patients (males = 138, females = 149, mean age = 77.8 +/- 6.9 years, range = 65-98) with diagnoses of VaD (n = 97), AD (n = 82) or NoCI (n = 108) were included in the study. A significantly higher APOE epsilon4 allele frequency was observed in AD patients compared to VaD and/or NoCI subjects, while no differences were found between VaD patients and subjects with NoCI (AD = 24.3%, VaD = 10.3, NoCI = 8.7, p < 0.05). Furthermore, a significantly lower APOE epsilon3 allele frequency was observed in AD patients compared to VaD and/or NoCI subjects but not between VaD and NoCI patients (AD = 71.3%, VaD = 80.9, NoCI = 83.4, p < 0.05). No significant differences were observed in the APOE epsilon2 allele (VaD = 8.8%, AD = 4.4, NoCI = 7.9, p = n.s.) among the 3 groups. CONCLUSIONS: In this population, the frequency of the APOE epsilon4 allele is lower in VaD than in AD.     

Apolipoprotein E epsilon4 allele frequency in vascular dementia

AIM: The aim of the study was to investigate whether possession of the epsilon4 allelic form of the apolipoprotein E (APOE) gene increases the risk of developing vascular dementia (VaD). METHODS: APOE allele and genotype frequencies were determined by PCR in 89 patients with possible and probable VaD and compared with those in 97 patients with possible and probable Alzheimer's disease (AD) of similar age of disease onset and ethnic background, and with 766 control subjects drawn from the same geographical region. RESULTS: The APOE epsilon4 allele frequency in all 97 patients with possible and probable AD was significantly higher (p < 0.001) than that in control subjects. However, the APOE epsilon4 allele frequency in all 89 patients with possible and probable VaD was also significantly higher (p < 0.001) than that in control subjects, but not significantly different from that in AD. The APOE epsilon4 allele frequency was similarly, and still significantly (p < 0.001), increased when only those patients with probable AD or probable VaD were considered. CONCLUSION: Possession of APOE epsilon4 allele increases the risk of VaD.     

阿尔茨海默病及血管性痴呆患者血清胆固醇及甲状腺激素变化的临床研究

目的探讨阿尔茨海默病(AD)和血管性痴呆(VaD)与血清胆固醇、甘油三脂、甲状腺激素的关系。方法对35例AD、35例VaD和16例健康对照组血清胆固醇、甘油三脂、甲状腺激素进行测定,并进行组间对比研究。结果 AD组和VaD组血清胆固醇、甘油三脂明显高于对照组(P<0．05),并且Va[)组甘油三脂水平与对照组相比差异更明显(P<0．01),而AD和VaD之间无显著性差异(P>0．05);AD组和VaD组血清总T4(TT4)水平明显高于健康对照组(P<0．01),而总T3(TT3)及TSH 3组之间无显著性差异。结论甲状腺激素代谢异常可能与 AD及VaD发病有关;血清胆固醇和甘油三脂增高与AD和VaD有明显的关系,降低胆固醇及血脂可能对AD和 VaD预防和治疗有益。     

阿尔茨海默病及血管性痴呆患者血清胆固醇、 Vit B12和叶酸变化的临床研究

目的探讨阿尔茨海默病(AD)和血管性痴呆(VaD)与血清胆固醇、血脂、Vit B12和叶酸的关系.方法对35例AD、35例VaD和16例健康对照组血清胆固醇、血脂、叶酸及Vit B12进行测定,并进行组间对比研究.结果AD组和VaD组血清胆固醇、甘油三酯明显高于对照组(P＜0.05),并且VaD组甘油三酯水平与对照组相比差异更明显(P＜0.01),而AD和VaD之间无显著性差异(P＞0.05),VaD组叶酸水平显著低于AD组和正常对照组(P＜0.05).Vit B12水平各组间相比无显著性差异(P＞0.05).结论血清叶酸水平降低可能与VaD发病有关,AD和VaD血清总胆固醇和甘油三酯明显增高,降低胆固醇及血脂可能对AD和VaD预防和治疗有益.     

Prospective Belgian study of neurodegenerative and vascular dementia: APOE genotype effects

OBJECTIVE: The authors conducted a prospective study of neurodegenerative and vascular dementia in Belgium. Strict diagnostic inclusion criteria were used to include well defined patients and controls. The results of apolipoprotein E (APOE) genotype effect on risk and clinical characteristics are presented. METHODS: APOE genotyping was performed in patients with probable Alzheimer's disease (AD) (n=504), frontotemporal dementia (FTD) (n=47), vascular dementia (VaD) (n=152), mixed dementia (n=132), mild cognitive impairment (MCI) (n=44), Parkinson's disease (PD) (n=30), dementia with Lewy bodies (DLB) (n=17), and multisystem atrophy (MSA)/progressive supranuclear palsy (PSP) (n=12). RESULTS: The APOE allele frequencies of this Belgian control population (epsilon 2: 6.9%; epsilon 3: 76.2%; epsilon 4: 16.9%) did not differ from those reported for other white populations. AD, MCI, and mixed dementia patients had higher APOE epsilon 4 (32.9%, 38.6%, and 28.4% respectively) and lower APOE epsilon 3 (62.2%, 53.4%, and 66.3%) frequencies compared with controls, whereas only AD and mixed dementia patients had lower APOE epsilon 2 frequencies (4.9% and 5.3%). Apart from a borderline significant different distribution of APOE allele frequencies in VaD patients compared with controls, no other differences were detected. The influence of APOE epsilon 4 on clinical features of dementia was limited to lower age at onset in AD patients and a less pronounced negative correlation between age at onset and number of epsilon 4 alleles in MCI and mixed dementia patients. CONCLUSIONS: This study confirmed the risk association between APOE epsilon 4 and AD. The observation that APOE epsilon 4 is associated with mixed dementia reflected the role of AD in the aetiopathogenesis of this condition. Although MCI is an aetiologically heterogeneous syndrome, the increased APOE epsilon 4 frequencies indicated that a large proportion of the MCI patients included in the study might be predisposed to develop AD.     

What is the relationship among atherosclerosis markers,apolipoprotein E polymorphism and dementia?

Evidence suggests the important role of vascular factors both in vascular dementia (VaD) and Alzheimer disease (AD) pathogenesis. However, the relationship between apolipoprotein E (APOE) polymorphism and markers of atherosclerosis is still controversial. The aim of the study was to investigate the interplay between APOE polymorphisms and atherosclerosis in patients with AD and VaD. In this cross-sectional study, 101 demented (68 AD and 33 VaD) patients underwent APOE genotyping and neck vessel ultrasound to evaluate carotid artery disease [intima-media thickness (IMT) and plaques]. Patients with AD carrying ɛ 4 allele presented increased IMT values with respect to non- ɛ 4 carriers and VaD patients, whereas no relation was found between APOE polymorphisms and the presence or grade of carotid plaques both in AD and VaD patients. The ɛ 4 APOE allele may promote intima-media thickening, interacting with other factors contributing to AD development.     

The effects of gender and CYP46 and apo E polymorphism on 24S-hydroxycholesterol levels in Alzheimer's patients treated with statins

To examine the effect of gender and polymorphisms of CYP46 and apo E on plasma levels of 24S-hydroxycholesterol in Alzheimer's disease (AD) patients and to determine whether these factors contribute to the variability in responses to statin treatment. Fifty-three AD patients had measurement of plasma levels of 24S-hydroxycholesterol, plasma and lipoprotein cholesterol and genotyping of CYP46 and apo E. Thirty-nine of the subjects subsequently participated in a statin trial for 6 weeks, and had a repetition of the baseline measurements. Baseline levels of 24S-hydroxycholesterol were higher in women than in men. There was a positive and significant correlation of plasma oxysterol levels with levels of total plasma cholesterol (women: r = .72, P < .0001; men: r = .47, P = .02) and non-HDL cholesterol (women: r = .68, P < .0001; men: r = 0.51, P = .01) (and LDL cholesterol) but not HDL cholesterol levels. There was no association of CYP46 or apo E polymorphisms with plasma levels of 24S-hydroxycholesterol. AD subjects treated with statins had a similar percent reduction in lathosterol, 24S-hydroxycholesterol, total cholesterol and non-HDL (and LDL) cholesterol regardless of gender and polymorphisms of CYP46. Subjects with the 4/4 polymorphism had less reduction in the ratios of 24S-hydroxycholesterol-LDL cholesterol. Women with AD had higher levels of plasma 24S-hydroxycholesterol levels than men. Women also showed a very strong correlation of plasma levels of 24S-hydroxycholesterol-to-total and non-HDL cholesterol. This may suggest that the oxysterol may be an important marker of AD risk instead of total cholesterol, as suggested by others. Polymorphisms of CYP46 or apo E do not explain levels of oxysterol or non-HDL cholesterol or the responsiveness to statin treatment in this study.     

Plasma cholesterol and risk for late-onset Alzheimer's disease

Alzheimer's disease (AD), the most common cause of dementia, is a progressive neurodegenerative disorder affecting millions of people worldwide. AD has a multifactorial origin, resulting from an interaction between genetic susceptibility and environmental risk factors. Genetic, epidemiological, experimental and clinical data strongly suggest that the metabolism of cholesterol has an important role in AD pathogenesis. Several studies have demonstrated that high concentrations of serum cholesterol increase the risk of AD. Statins, drugs that reduce cholesterol levels, have been investigated as a possible treatment for AD. However, the literature is not exempt of contradictory results. In this article, we review a recent article by Reitz et al. demonstrating that higher levels of high-density lipoprotein cholesterol, total cholesterol and non-high-density lipoprotein cholesterol are associated with lower risk of AD. In addition, we discuss the current state of knowledge regarding the relationship between plasma cholesterol and AD, stressing the need for understanding the molecular mechanisms behind this association.     

The association between APOE and dementia does not seem to be mediated by vascular factors

OBJECTIVE: The effect of APOE on dementia may be mediated through dyslipidemia and atherogenesis through its effect on cholesterol metabolism. The authors investigated this possibility among aged survivors from the UK Medical Research Council Trial of the Treatment of Hypertension in Older Adults. DESIGN: A total of 370 of 657 survivors from an initial cohort of 1,088 recruited into the trial between 1983 and 1985 were traced in 1994 and agreed to be screened for dementia. Blood samples were analyzed for APOE genotype and serum fibrinogen. Cholesterol level, smoking behavior, blood pressure, body mass index, and EKG recordings had been measured at recruitment 10 to 12 years earlier. Odds ratios (ORs) for the association between APOE epsilon4/* and both AD and dementia were estimated and adjusted incrementally for the effect of age and premorbid intelligence, cholesterol, other risk factors for vascular disease, and EKG evidence of cardiovascular disease. RESULTS: The authors diagnosed 24 cases of National Institute of Neurological and Communicative Disorders and Stroke AD from 41 cases of dementia. The crude OR for the association between APOE epsilon4/* and AD was 3.40 (95% CI 1.30 to 8.91). APOE genotype was associated with serum cholesterol level, and there was a nonsignificant trend for an association with smoking behavior. After adjusting for these and all other vascular risk factors and vascular disease variables listed earlier, the OR for the association between APOE epsilon4/* and AD increased to 4.81 (1.60 to 14.4). CONCLUSION: Presence of APOE epsilon4/* seems to increase the risk for dementia and AD independently of its effect on dyslipidemia and atherogenesis.     

Vascular risk factors for incident Alzheimer disease and vascular dementia: the Cache County study

Vascular risk factors for Alzheimer disease (AD) and vascular dementia (VaD) have been evaluated; however, few studies have compared risks by dementia subtypes and sex. We evaluated relationships between cardiovascular risk factors (hypertension, high cholesterol, diabetes mellitus, and obesity), events (stroke, coronary artery bypass graft surgery, and myocardial infarction), and subsequent risk of AD and VaD by sex in a community-based cohort of 3264 Cache County residents aged 65 or older. Cardiovascular history was ascertained by self-report or proxy-report in detailed interviews. AD and VaD were diagnosed using standard criteria. Estimates from discrete-time survival models showed no association between self-reported history of hypertension and high cholesterol and AD after adjustments. Hypertension increased the risk of VaD [adjusted hazard ratio (aHR) 2.42, 95% confidence interval (CI) 0.95-7.44]. Obesity increased the risk of AD in females (aHR 2.23, 95% CI 1.09-4.30) but not males. Diabetes increased the risk of VaD in females after adjustments (aHR 3.33, 95% CI 1.03-9.78) but not males. The risk of VaD after stroke was increased in females (aHR 16.90, 95% CI 5.58-49.03) and males (aHR 10.95, 95% CI 2.48-44.78). The results indicate that vascular factors increase risks for AD and VaD differentially by sex. Future studies should focus on specific causal pathways for each of these factors with regard to sex to determine if sex differences in the prevalence of vascular factors have an influence on sex differences in dementia risk.     

中青年人脑卒中与血脂关系的研究

目的 探讨血脂与中青年人脑卒中的关系。方法 检测了206例中青年脑卒中患者及80例对照者的甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL－C）、低密度脂蛋白胆固醇（LDL－C）、载脂蛋白A－I（ApoA-I)、载脂蛋白B100（ApoB100)和脂蛋白（a)[Lp(a)]血清含量。结果 脑梗死组TG、TC、LD-L－C、ApoB100及Lp(a)水平显著高于对照组,Lp(a)水平亦高于脑出血组,异常的血脂成分随年龄变化而发生改变;皮层动脉区脑梗死组Lp(a)水平显著高于穿通动脉区脑梗死组;脑出血组血脂指标与对照组比较差异无显著。结论 血脂代谢紊乱是中青年人脑梗死的危险因素。     

Differences in risk factors for dementia with neurodegenerative traits and for vascular dementia

In 229 patients with dementia and in 144 control subjects, polymorphisms of apolipoprotein E (ApoE), low-density-lipoprotein (LDL)-receptor-related protein, alpha(2)-macroglobulin, interleukin (IL) 1beta, angiotensin-converting enzyme and of methylene tetrahydrofolate reductase genes were investigated. In plasma, antibodies against Chlamydia pneumoniae and lipids were determined. Dementia was classified as probable Alzheimer's disease (AD), probable dementia of vascular origin (VaD) and mixed dementia (MD). An association of the disease with ApoE and IL-1beta polymorphism and increased levels of LDL cholesterol were observed in AD and in MD but not in VaD.