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HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction
Open accessAbstract
High mobility group box protein 1 (HMGB1) is a ubiquitous nuclear protein released by glia and neurons upon inflammasome activation and activates receptor for advanced glycation end products (RAGE) and toll-like receptor (TLR) 4 on the target cells. HMGB1/TLR4 axis is a key initiator of neuroinflammation. In recent days, more attention has been paid to HMGB1 due to its contribution in traumatic brain injury (TBI), neuroinflammatory conditions, epileptogenesis, and cognitive impairments and has emerged as a novel target for those conditions. Nevertheless, HMGB1 has not been portrayed as a common prognostic biomarker for these HMGB1 mediated pathologies. The current review discusses the contribution of HMGB1/TLR4/RAGE signaling in several brain injury, neuroinflammation mediated disorders, epileptogenesis and cognitive dysfunctions and in the light of available evidence, argued the possibilities of HMGB1 as a common viable biomarker of the above mentioned neurological dysfunctions. Furthermore, the review also addresses the result of preclinical studies focused on HMGB1 targeted therapy by the HMGB1 antagonist in several ranges of HMGB1 mediated conditions and noted an encouraging result. These findings suggest HMGB1 as a potential candidate to be a common biomarker of TBI, neuroinflammation, epileptogenesis, and cognitive dysfunctions which can be used for early prediction and progression of those neurological diseases. Future study should explore toward the translational implication of HMGB1 which can open the windows of opportunities for the development of innovative therapeutics that could prevent several associated HMGB1 mediated pathologies discussed herein.
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“elevated HMGB1 levels are found in the brain and CSF of AD patients and aged rodents and correlate with disease severity. 88 , 89 , 90”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [90]
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Metadata
- Authors
- Paudel, Y. N., Shaikh, M. F., Chakraborti, A., Kumari, Y., Aledo-Serrano, Á., Aleksovska, K., Alvim, M. K. M., & Othman, I.
- Affiliations
- Monash University Malaysia (MY)
- University of Alabama at Birmingham (US)
- Ss. Cyril and Methodius University in Skopje (MK)
- Universidade Estadual de Campinas (UNICAMP) (BR)
- Corresponding author
- Shaikh, Mohd. Farooq
- ORCID
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-09-11
- Volume
- 12
- Pages
- 628-628
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC6142787
- OpenAlex
- W2889849480
- Cited by
- 311
- References
- 166
- Citations by year
- 2026: 38 · 2025: 29 · 2024: 36 · 2023: 33 · 2022: 56 · 2021: 45 · 2020: 53 · 2019: 19 · 2018: 2
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Monash University Research Portal (Monash University) (submittedVersion, cc-by)
- Charles Sturt University Research Output (CRO) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Monash University
- Monash University Malaysia
- Jaypee University of Information Technology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- HMGB1, traumatic brain injury, neuroinflammation, epileptogenesis, cognitive impairment, TLR4, RAGE, inflammasome, prognostic factors, neuroinflammatory disorders
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