BACKGROUND AND AIMS: Alzheimer’s disease (AD) is a multifactorial disease conditioned by genes (70%) and environment (30%), characterized by brain deposition of amyloid-β and neurofibrillary tangles. An involvement of over 20 genes (including APOE) and dozens of microRNAs (e.g. miR-107) has been previously described in the pathogenesis of AD. APOE has 3 common variants: protective – ε2, neutral – ε3 and pathogenic – ε4. The miR-107, associated with amyloid cascade, seems to be a promising AD plasma biomarker, whose downregulation has been demonstrated in the early stage of the disease. Though miR-132 has been linked with apoptosis of neurons and miR-138 with tau hyperphosphorylation, their role in AD remain unclear, and neither of these miRNA has been previously associated with APOE. The aim of the study was the analysis of APOE genotypes and the expression of three miRNAs: miR-107, -132, -138 in patients with AD and in control subjects, both related and unrelated to AD cases. METHODS: The DNA from 100 subjects (aged 47–83), including 42 patients with AD and 15 related and 43 unrelated controls of the same age was genotyped by “mismatch primer” qPCR. The subsequent expression analysis of miR-107, -132 and -138 in the plasma of ten subjects was performed by qPCR. RESULTS: Our study have shown that the miR-107 was significantly downregulated in AD patients (P<0.05) comparing to related controls, but did not reach significance as compared to unrelated controls. The downregulation of miR-132 was not statistically significant as compared to related and unrelated subjects. Expression of miR-138 in AD was decreased only as compared to relatives. Subsequently, the presence of two APOE ε4 alleles in AD patient and at least one ε4 copy in the controls was associated with altered expression of the analyzed miRNAs. CONCLUSIONS: It appears that in the course of AD the expression of miR-107, -132 and -138 depends on the APOE genotype.
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