Journal
LANCET NEUROLOGY
Volume 18, Issue 11, Pages 1058-1066Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S1474-4422(19)30078-X
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Funding
- National Key Research and Development Program of China [2018YFC1312200]
- National Science Foundation of China [91642205, 81830038]
- Barrow Neurological Foundation
- Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing, China
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Stroke, including acute ischaemic stroke and intracerebral haemorrhage, results in neuronal cell death and the release of factors such as damage-associated molecular patterns (DAMPs) that elicit localised inflammation in the injured brain region. Such focal brain inflammation aggravates secondary brain injury by exacerbating blood-brain barrier damage, microvascular failure, brain oedema, oxidative stress, and by directly inducing neuronal cell death. In addition to inflammation localised to the injured brain region, a growing body of evidence suggests that inflammatory responses after a stroke occur and persist throughout the entire brain. Global brain inflammation might continuously shape the evolving pathology after a stroke and affect the patients' long-term neurological outcome. Future efforts towards understanding the mechanisms governing the emergence of so-called global brain inflammation would facilitate modulation of this inflammation as a potential therapeutic strategy for stroke.
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