This Research Topic is part of the Brain hypoxia and ischemia: new insights into neurodegeneration and neuroprotection series:
Brain hypoxia and ischemia: new insights into neurodegeneration and neuroprotectionNormal brain functions depend immensely on oxygen, hence making neuronal cells vulnerable to reduced oxygen levels. Insufficient oxygen supply (hypoxia) or reduced blood flow to the brain (ischemia) leads to neurodegeneration, cognitive impairment, seizures, and other neurological disabilities. Ischaemic stroke is the third leading cause of death in Western countries behind heart failure and cancer. Hypoxia has a significant effect on cellular functions with an immediate response by membrane lipids, enzymes, and mitochondrial remodeling, and with long-term changes in gene expression and protein synthesis. Accumulated data suggest that impaired vascular health and reduced oxygen supply to the brain affect behavior and cognition of individuals, which are linked to the pathogenesis of various neurodegenerative disorders, including vascular dementia and Alzheimer’s disease. Hypoxia during the prenatal period or in labour significantly affects brain development and functions and predisposes to various cognitive abnormalities in later life.
In the last 10 years, increased numbers of hypoxia studies including the works of 2019 Nobel Prize winners William Kaelin, Sir Peter Ratcliffe, and Gregg Semenza have given us a better understanding of the molecular mechanisms by which hypoxia affects cell functions and suggests therapeutic targets in preventing the pathological outcomes of hypoxic and ischemic insults to the brain. Despite all these studies, there are still no widely accepted pharmacological treatments available to reduce cell death in the ischaemic/hypoxic brain. Nevertheless, there are endogenous mechanisms allowing the central nervous system to withstand hypoxia or ischemia for a limited amount of time, a phenomenon called primary hypoxic–ischaemic tolerance. Various modes of hypoxia pre- and postconditioning have been developed to increase brain resistance not only to hypoxic/ischaemic insults but also to other injurious factors including stress, and a number of genes have been identified which contribute to hypoxia-induced tolerance.
With COVID-19 pandemics affecting the world from early 2020, it is becoming clear that hypoxia is one of the factors which accompanies this systemic disease, with neurologic manifestations being reported in patients not only with severe conditions but also with mild symptoms.
We are very pleased that the first issue of the Research Topic "Brain hypoxia and ischemia: new insights into neurodegeneration and neuroprotection" has been well received by the scientific community and we are happy to invite scientists to contribute to its second edition.
This Research Topic welcomes articles and review papers in the areas of
i) brain membrane biochemistry, including lipids, proteins, channels, and processing of complex membrane proteins;
ii) molecular biology (effects of hypoxia and ischemia on gene expression, role of miRNAs);
iii) role of mitochondria in urgent adaptation to hypoxia;
iv) morphological changes in the brain after hypoxia or ischemia;
v) perivascular status of the brain and functions of the blood-brain barrier;
vii) role of hypoxia and ischemia in development of cognitive functions and neurological disorders;
viii) protective mechanisms of hypoxic pre- and postconditioning and their possible therapeutic applications;
ix) therapeutic targets in preventing hypoxic and ischemic brain insults and the severity of their outcomes;
x) COVID-19 and its role in hypoxia-related brain disorders.