Tau Protein, α-synuclein, and Amyloid Precursor Protein Processing Genes in the Frontal Cortex of an Ischemic Alzheimer's Disease Model

Introduction: Information regarding the changes in tau protein, α-synuclein, and amyloid precursor protein processing genes in the frontal cortex post-ischemia, cannot be found in literature We decided to examine the expression of these genes in rats after 10-min of cerebral ischemia with survival of 2-30 days and 6-24 months. Methods: Gene expression was assessed by RT-PCR. The relative quantity (RQ) of the studied gene was shown using ΔCT, and the last value was shown as RQ = 2-ΔΔCT. Results: Two days, 12-18 months post-ischemia, the amyloid precursor protein gene was significantly overexpressed. However, the α-secretase gene was significantly overexpressed on day 2 and 12 months post-ischemia. At 1 year post-ischemia β-secretase gene was significantly overexpressed. Presenilin 1 and 2 genes at 2 days, 12 months post-ischemia were significantly overexpressed. At 12-18 months post-ischemia tau protein gene was significantly overexpressed, and at other times it was below control. At 2 days and 12-18 months post-ischemia, the α-synuclein gene was significantly overexpressed, and at other times it was below control. Discussion: The data indicate that after cerebral ischemia, there is no activation of genes that could influence amyloid production in the frontal cortex. However, the data indicate significant activation of tau protein and α-synuclein genes. Conclusion: We revealed non-amyloidogenic metabolism of amyloid precursor protein in the frontal cortex post-ischemia. Moreover, the results showed increased expression of tau protein and α- synuclein genes at 12-18 months post-ischemia, suggesting the involvement of these genes in neurodegenerative processes in the frontal cortex.