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Background: Amyloid deposition in the brain is an early event in Alzheimer’s disease (AD), but a dysfunction of the blood-brain barrier or a disturbance in the metabolism of folate and homocysteine (Hcy) may affect the development of dementia. We investigated if the concentrations of folate and Hcy would be modified in cerebrospinal fluid (CSF) of clinically diagnosed AD patients. Methods: We included 70 AD patients, 33 patients with another type of dementia (nAD) and 30 age-matched control subjects. Plasma Hcy was assayed as well as Hcy, folate, Aβ1-42 and T-tau in CSF. We used ANOVAs for comparison between groups, and then pairwise comparisons by Wilcoxon tests with Bonferroni-corrected p values. Correlations were tested with the Spearman’s rank test. Results: Levels of Aβ1-42, T-tau and folates in CSF were significantly different between groups, but not Hcy. In addition, the average folate in CSF was lower in AD patients compared with controls (18.7 ± 2.4 vs. 20.3 ± 1.7 nmol/l, Bonferroni-corrected p value < 0.02). There was no correlation between Aβ1-42 or T-tau and folate or Hcy in CSF, regardless of the group. In the AD group, there was a significant inverse correlation between Hcy and folate in CSF (ρ = –0.63, p < 0.0001), whereas in the nAD group, a significant correlation was found for Hcy between plasma and CSF (ρ = 0.59, p < 0.0005). Conclusion: The concentration of folate in CSF was found to be decreased in AD patients. These findings support the hypothesis of a possible role of folate in the onset or worsening of AD.

Background: Alzheimer’s disease (AD) is the leading cause of dementia. Currently, no definitive diagnostic test for AD exists. Cerebrospinal fluid (CSF) concentrations of amyloid β (Aβ1-42) peptides and total tau proteins (T-tau) may serve as biomarkers for AD. Aim: The objective of this study was to investigate the usefulness of CSF Aβ1-42 and T-tau analyses in the diagnosis of AD with Tunisians. Methods: We focused on three groups originating from Central Tunisian that matched in age (range 48–85): healthy controls (n = 53), AD patients (n = 93) and non-Alzheimer (nAD) dementia (n = 35) patients. Aβ1-42 and T-tau levels were measured in CSF by sandwich enzyme-linked immunosorbent assay. Results: The ratio of T-tau/Aβ1-42 at baseline yielded a sensitivity of 85.3% for detection of AD and the specificity was 84.8% to differentiate controls and nAD dementia. Conclusion: Our findings confirm the use of T-tau/Aβ1-42 ratio in the discrimination of AD patients from all other patients.

Background: Apolipoprotein A1 (apoA1) is the major apolipoprotein constituent of the high-density lipoprotein (HDL) and is involved in reverse cholesterol transport. Variation in the apoA1 gene might influence the function of the protein and, thus, brain cholesterol metabolism, leading to an increased risk for Alzheimer’s disease (AD). Aim: In the current report, we investigated the role of the functional apoA1 polymorphism (–75 G/A) as a genetic risk factor for AD in a Tunisian population. Methods: 173 AD patients and 150 healthy controls were studied. Results: No association was found between this genetic variation in apoA1 gene and the risk of AD. The presence of the (–75 G/A) A allele appeared, however, to be associated with lower levels of cerebrospinal fluid Aβ42 and HDL cholesterol levels in sera. Conclusion: Our data support the observation that apoA1 polymorphism influences cholesterol metabolism and Aβ42 deposition in the brain.

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Alzheimer's disease (AD) is the leading cause of dementia. Several studies indicate a possible relationship between different genes and Alzheimer's disease. To further investigate, we have analyzed the association between the bleomycin hydrolase (BLMH) and apolipoprotein E (ApoE) polymorphisms in 93 AD patients and age- and sex-matched 113 controls from the Tunisian population. The frequency of ApoE epsilon 4 allele was found to differ significantly in AD patients compared to the control [29.5% vs. 8.8 (χ (2) = 26, df = 1, p < 0.001)] leading to an increased risk of AD in subjects with this allele (OR = 3.29, 95% CI = 1.7-6.5; p = 0.001]. This risk was found to decrease from OR = 8.4, CI = 3.3-23; p < 0.001 in subjects less than 75 years old to OR = 1.2, CI = 1.031-14; p = 0.0297 in subjects 75 years and older. No association was observed between carrying the BLMH-G genotype and AD in ε4 negative or positive subjects.