Mechanisms of Neurovascular Dysfunction in Acute Ischemic Brain

Abstract

The neurovascular unit is now well accepted as a conceptual framework for investigating the mechanisms of ischemic stroke. From a molecular and cellular perspective, three broad mechanisms may underlie stroke pathophysiology – excitotoxicity, oxidative stress and inflammation. To date, however, most investigations of these basic mechanisms have focused on neuronal responses. In this mini-review, we ask whether these mechanisms of excitotoxicity, oxidative stress and inflammation can also be examined in terms of non-neuronal interactions in the neurovascular unit, including the release of extracellular vesicles for cell-cell signaling.

Repeated formaldehyde inhalation impaired olfactory function and changed SNAP25 proteins in olfactory bulb

“…14 SNAP25, a component in the SNARE complex, decreased in the hippocampus after formaldehyde inhalation, which may be responsible for learning and memory impairment. 15 We hypothesize that SNAP25 changes may lead to olfactory function impairment as a result of repeated formaldehyde inhalation exposure. This study contributes to the understanding of brain damage caused by formaldehyde inhalation exposure.…”

Neurovascular Oxidative Stress and Autonomic Modulation Contributing to QT Interval Variations in Acute Large Artery Ischemic Stroke

“…This result indicates degree of oxidative stress occurring on D1 stroke resulting from brain injury. As many previous reports have mentioned that further brain injury causes in turn, more glia activation [36,37]. Moreover, heart rate in L QTc increases and shows a significant difference compared with S QTc and N QTc.…”

“…Oxidative stress causes neuronal necrosis and death. During ischemic stroke, progressive neuron death is closely related with glia activation and neurovascular unit especially cerebral endothelium which both of them play a vital role for energy supply and reducing glutamate cascade toxicity [36]. Neurovascular-glia interaction is an important mechanism during ischemia especially under overwhelmed oxidative stress condition.…”

“…Neurovascular-glia interaction is an important mechanism during ischemia especially under overwhelmed oxidative stress condition. Nitric oxide is well known vasomotor tone mediator from vascular endothelium and also neuromodulator of glutamate release in brain [36]. Recently, it has been reported that NO plays a vital role at medullary neuron with H 2 O 2 as neuromodulator of redox signal from ROS formation and they are related with sympathetic activity drive at medulla for central hypertension [37].…”

“…Recently, it has been reported that NO plays a vital role at medullary neuron with H 2 O 2 as neuromodulator of redox signal from ROS formation and they are related with sympathetic activity drive at medulla for central hypertension [37]. Recently, NO and H 2 O 2 are coupled relaxing factors in brain corresponding with increasing cerebral blood flow during cerebrovascular reactivity in normal and lacunar stroke (small artery stroke) [19,[32][33][34][35][36][37][38]. Both of them are gases that diffuse rapidly to cerebrospinal fluid and then in blood circulation within 30 seconds as assessed by cerebrovascular reactivity [38].…”