Abstract
Recent evidence suggests that transient ischemia of the brain with reperfusion in humans and animals is associated with the neuronal accumulation of neurotoxic molecules associated with Alzheimer’s disease, such as all parts of the amyloid protein precursor and modified tau protein. Pathological changes in the amyloid protein precursor and tau protein at the protein and gene level due to ischemia may lead to dementia of the Alzheimer’s disease type after ischemic brain injury. Some studies have demonstrated increased tau protein immunoreactivity in neuronal cells after brain ischemia-reperfusion injury. Recent research has presented many new tau protein functions, such as neural activity control, iron export, protection of genomic DNA integrity, neurogenesis and long-term depression. This review discusses the potential mechanisms of tau protein in the brain after ischemia, including oxidative stress, apoptosis, autophagy, excitotoxicity, neurological inflammation, endothelium, angiogenesis and mitochondrial dysfunction. In addition, attention was paid to the role of tau protein in damage to the neurovascular unit. Tau protein may be at the intersection of many regulatory mechanisms in the event of major neuropathological changes in ischemic stroke. Data show that brain ischemia activates neuronal changes and death in the hippocampus in a manner dependent on tau protein, thus determining a new and important way to regulate the survival and/or death of post-ischemic neurons. Meanwhile, the association between tau protein and ischemic stroke has not been well discussed. In this review, we aim to update the knowledge about the proteomic and genomic changes in tau protein following ischemia-reperfusion injury and the connection between dysfunctional tau protein and ischemic stroke pathology. Finally we present the positive correlation between tau protein dysfunction and the development of sporadic Alzheimer’s disease type of neurodegeneration.
Highlights
Ischemic brain injury in the human clinic is the second leading cause of death and the third leading cause of physical disability, and may soon become the main cause of Alzheimer’s disease type dementia, and, currently, brain ischemia is proposed to be a risk factor for developing Alzheimer’s disease [1,2,3,4,5,6]
Data show that brain ischemia activates neuronal changes and death in the hippocampus in a manner dependent on tau protein, determining a new and important way to regulate the survival and/or death of post-ischemic neurons
This review shows the response of the tau protein gene and its products to brain ischemia with recirculation (Figures 2 and 3)
Summary
Ischemic brain injury in the human clinic is the second leading cause of death and the third leading cause of physical disability, and may soon become the main cause of Alzheimer’s disease type dementia, and, currently, brain ischemia is proposed to be a risk factor for developing Alzheimer’s disease [1,2,3,4,5,6]. Previous brain damage associated with ischemia and reperfusion may further increase the likelihood of developing dementia associated with Alzheimer’s disease, increasing the extent of post-ischemic changes, through the proteomic and genomic cascade associated with Alzheimer’s disease [26,27,28,29,30,31,32,33,34,35,36,37]. We will present the contribution of tau protein after ischemia to the development of sporadic Alzheimer’s disease type of neurodegeneration, focusing on both changes in its structure and the expression of its gene after brain ischemia insult. The hyper-phosphorylated state is the pathological condition of tau protein in post-ischemic brains It decreases the affinity of tau protein for the microtubules by disrupting the binding balance [47].
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