TNF-related apoptosis inducing ligand (TRAIL), a member of the TNF superfamily released by microglia, appears to be involved in the induction of apoptosis following focal brain ischemia.
We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia.
Blood-brain barrier (BBB) breakdown and inflammatory responses are the major causes of tissue-type plasminogen activator (tPA)-induced hemorrhagic transformation (HT), while high-mobility group box 1 (HMGB1) exacerbates inflammatory damage to BBB during the process of brain ischemia/reperfusion.
We have investigated the relationship between hippocampal ischemia and Alzheimer's disease by means of a transient 10-min global brain ischemia in rats and determining the effect on Alzheimer's disease tau protein gene expression during 2, 7 and 30 days post injury.
Recent knowledge on the activation of Alzheimer's disease-related genes and proteins-e.g., amyloid protein precursor and tau protein-as well as brain ischemia and Alzheimer's disease neuropathology indicate that similar processes contribute to neuronal death and disintegration of brain tissue in both disorders.
Data show that brain ischemia activates neuronal changes and death in the CA3 region of the hippocampus in a manner dependent on amyloid and tau protein, thus determining a new and important way to regulate the survival and/or death of ischemic neurons.
Thus, we hypothesize that the changes in pattern of phosphorylation of tau protein are critical to microtubule function especially in neurons, and contribute to the neurodegeneration following brain ischemia-reperfusion episodes with Alzheimer's disease phenotype.
The authors and other groups have reported that the expression of RAGE increases after brain ischemia and subarachnoid hemorrhage (SAH), and deletion of RAGE or overexpression of sRAGE improves neuronal survival.
MGF has been shown to activate satellite cells in muscle resulting in hypertrophy or regeneration, and functions as a neuroprotectant in brain ischemia.
Insulin-like growth factor-1 (IGF-1) and erythropoietin (EPO) are induced in brain cells after brain ischemia and show synergistic neuroprotective effects.
Serum Levels of S100b and NSE Proteins in Patients with Non-Transfusion-Dependent Thalassemia as Biomarkers of Brain Ischemia and Cerebral Vasculopathy.
Notably, antimiR-103-1 prevented NCX1 protein downregulation induced by the increase in miR-103-1 after brain ischemia, thereby reducing brain damage and neurological deficits.
The efferocytic activity of brain macrophages were verified by immunohistochemistry, wherein Iba1-labeled microglia/macrophages effectively cleared apoptotic neurons in the infarct during the subacute stage after brain ischemia.
Collectively, these results demonstrate that REST, by regulating NCX1 expression, may represent a potential druggable target for the treatment of brain ischemia.
In view of these considerations, AIF-2 might represent an ideal strategy to avoid AIF-1 associated neurotoxicity, and could be tested against brain ischemia in animal models.
The ability of PKCɛ activation to regulate AMPA receptors (AMPARs) remains unexplored despite the role of AMPARs in excitotoxicity after brain ischemia.
The present study aimed to compare the expression of phosphatidylinositol 3‑kinase (PI3‑K), mammalian target of rapamycin (mTOR) and Beclin‑1 between the hippocampi of normal rats and intermittent ischemic rats following whole brain ischemia/reperfusion (I/R), and investigate the role of the PI3K‑mTOR autophagy pathway in rat nerve damage following intermittent hypoxia (IH)‑aggravated whole brain ischemia.