Abstract
Post-ischemic brain damage is associated with the deposition of folding proteins such as the amyloid and tau protein in the intra- and extracellular spaces of brain tissue. In this review, we summarize the protein changes associated with Alzheimer’s disease and their gene expression (amyloid protein precursor and tau protein) after ischemia-reperfusion brain injury and their role in the post-ischemic injury. Recent advances in understanding the post-ischemic neuropathology have revealed dysregulation of amyloid protein precursor, α-secretase, β-secretase, presenilin 1 and 2, and tau protein genes after ischemic brain injury. However, reduced expression of the α-secretase in post-ischemic brain causes neurons to be less resistant to injury. In this review, we present the latest evidence that proteins associated with Alzheimer’s disease and their genes play a key role in progressive brain damage due to ischemia and reperfusion, and that an ischemic episode is an essential and leading supplier of proteins and genes associated with Alzheimer’s disease in post-ischemic brain. Understanding the underlying processes of linking Alzheimer’s disease-related proteins and their genes in post-ischemic brain injury with the risk of developing Alzheimer’s disease will provide the most significant goals for therapeutic development to date.
Highlights
Most studies on the consequences of cerebral ischemia have been conducted in rodents
The results show that ischemic brain damage causes neuronal death in the hippocampus and medial temporal cortex in an amyloid-dependent mechanism, defining a new and very important process that regulates neuronal survival and/or death after ischemia (Tables 1–3) [62,63,64,65]
Two-sided damage to the above-mentioned regions causes a short-term memory deterioration, which leads to the inability to create new memories. It is well-known that amyloid and hyperphosphorylated tau protein are closely associated with neurodegeneration and cognitive impairment in Alzheimer’s disease
Summary
Most studies on the consequences of cerebral ischemia have been conducted in rodents. Ischemic changes in the brain showed signs of progressive neurodegeneration that developed slowly over a long period of time within recirculation after an episode of cerebral ischemia [2]. Brain autopsy carried out within 1–2 years after ischemia showed the features of hydrocephalus [1,2,26] with the widening of the ventricles and the subarachnoid space around the cerebral hemispheres [1] During this time, general atrophy of the hippocampus with very narrow cerebral cortex was observed [1,2,4,26,27]. We present here changes in proteins associated with Alzheimer’s disease and the expression of their genes (amyloid protein precursor, and tau protein) after ischemic-reperfusion injury of the brain and their role in post-ischemic neurodegeneration. We present the latest evidence that Alzheimer’s disease-associated proteins and their genes play an important role in the progression of brain neurodegeneration after cerebral ischemia
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