Abstract
Current evidence indicates that postischemic brain injury is associated with the accumulation of folding proteins, such as amyloid and tau protein, in the intra- and extracellular spaces of neuronal cells. In this review, we summarize protein changes associated with Alzheimer’s disease and their gene expression (amyloid protein precursor and tau protein) after brain ischemia, and their roles in the postischemic period. Recent advances in understanding the postischemic mechanisms in development of neurodegeneration have revealed dysregulation of amyloid protein precursor, α-, β- and γ-secretase and tau protein genes. Reduced expression of the α-secretase gene after brain ischemia with recirculation causes neuronal cells to be less resistant to injury. We present the latest data that Alzheimer’s disease-related proteins and their genes play a crucial role in postischemic neurodegeneration. Understanding the underlying processes of linking Alzheimer’s disease-related proteins and their genes in development of postischemic neurodegeneration will provide the most significant goals to date for therapeutic development.
Highlights
Brain ischemia is one of the most common forms of neurodegeneration, with a series of pathological molecular processes that occur during and after ischemia and gradually spread to various brain structures
We present changes in expression of genes involved in the amyloidogenic metabolism of the amyloid protein precursor, which are associated with the production of amyloid in the postischemic brain
Progress in understanding new key processes induced by brain ischemia with recirculation, like changes in the genotype and phenotype of the Alzheimer’s disease type, which are not yet fully explained, may help develop strategies for prevention and treatment against neurodegeneration induced by ischemia
Summary
Brain ischemia is one of the most common forms of neurodegeneration, with a series of pathological molecular processes that occur during and after ischemia and gradually spread to various brain structures. In the CA1 region of the hippocampus, expression of the presenilin 1 gene increased 2–7 days after ischemia but 30 days postischemia the expression of this gene was below the control values (Table 3) [39]. In the CA3 area of the hippocampus, expression of the presenilin 1 gene increased 2–7 days postischemia, and was below the control values 30 days after ischemia (Table 3) [38]. In the medial temporal cortex, the expression of the presenilin 1 gene oscillated around the control values during 2, 7 and 30 days postischemia (Table 3) [41]. In the CA1 area of the hippocampus, expression of the presenilin 2 gene increased 2–7 days postischemia but, in contrast, 30 days following ischemia the expression of this gene was below the control values (Table 4) [39].
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