Recent data suggest that post-ischemic brain neurodegeneration in humans and animals is associated with the modified
tau protein in a manner typical of
Alzheimer's disease neuropathology. Pathological changes in the
tau protein, at the gene and
protein level due to
cerebral ischemia, can lead to the development of
Alzheimer's disease-type neuropathology and
dementia. Some studies have shown increased
tau protein staining and gene expression in neurons following
ischemia-reperfusion
brain injury. Recent studies have found the
tau protein to be associated with oxidative stress, apoptosis, autophagy, excitotoxicity,
neuroinflammation, blood-brain barrier permeability,
mitochondrial dysfunction, and impaired neuronal function. In this review, we discuss the interrelationship of these phenomena with post-ischemic changes in the
tau protein in the brain. The
tau protein may be at the intersection of many pathological mechanisms due to severe neuropathological changes in the brain following
ischemia. The data indicate that an episode of
cerebral ischemia activates the damage and death of neurons in the hippocampus in a
tau protein-dependent manner, thus determining a novel and important mechanism for the survival and/or death of neuronal cells following
ischemia. In this review, we update our understanding of proteomic and genomic changes in the
tau protein in post-ischemic
brain injury and present the relationship between the modified
tau protein and post-ischemic neuropathology and present a positive correlation between the modified
tau protein and a post-ischemic neuropathology that has characteristics of
Alzheimer's disease-type neurodegeneration.