TY - JOUR
T1 - High Mobility Group Box-1 (HMGB1), a key mediator of cognitive decline in neurotrauma with a potential for targeted therapy
T2 - A comprehensive review
AU - Navaseelan, Locshiny
AU - Retinasamy, Thaarvena
AU - Shaikh, Mohd Farooq
AU - Arulsamy, Alina
N1 - © 2024 The Author(s). Published by IMR Press.
PY - 2024/9/20
Y1 - 2024/9/20
N2 - Neurotrauma plays a significant role in secondary injuries by intensifying the neuroinflammatory response in the brain. High Mobility Group Box-1 (HMGB1) protein is a crucial neuroinflammatory mediator involved in this process. Numerous studies have hypothesized about the underlying pathophysiology of HMGB1 and its role in cognition, but a definitive link has yet to be established. Elevated levels of HMGB1 in the hippocampus and serum have been associated with declines in cognitive performance, particularly in spatial memory and learning. This review also found that inhibiting HMGB1 can improve cognitive deficits following neurotrauma. Interestingly, HMGB1 levels are linked to the modulation of neuroplasticity and may offer neuroprotective effects in the later stages of neurotraumatic events. Consequently, administering HMGB1 during the acute phase may help reduce neuroinflammatory effects that lead to cognitive deficits in the later stages of neurotrauma. However, further research is needed to understand the time-dependent regulation of HMGB1 and the clinical implications of treatments targeting HMGB1 after neurotrauma.
AB - Neurotrauma plays a significant role in secondary injuries by intensifying the neuroinflammatory response in the brain. High Mobility Group Box-1 (HMGB1) protein is a crucial neuroinflammatory mediator involved in this process. Numerous studies have hypothesized about the underlying pathophysiology of HMGB1 and its role in cognition, but a definitive link has yet to be established. Elevated levels of HMGB1 in the hippocampus and serum have been associated with declines in cognitive performance, particularly in spatial memory and learning. This review also found that inhibiting HMGB1 can improve cognitive deficits following neurotrauma. Interestingly, HMGB1 levels are linked to the modulation of neuroplasticity and may offer neuroprotective effects in the later stages of neurotraumatic events. Consequently, administering HMGB1 during the acute phase may help reduce neuroinflammatory effects that lead to cognitive deficits in the later stages of neurotrauma. However, further research is needed to understand the time-dependent regulation of HMGB1 and the clinical implications of treatments targeting HMGB1 after neurotrauma.
KW - HMGB1 Protein/metabolism
KW - Humans
KW - Animals
KW - Cognitive Dysfunction/etiology
KW - Brain Injuries, Traumatic/complications
KW - Molecular Targeted Therapy/methods
KW - Hippocampus/metabolism
KW - Neuronal Plasticity/drug effects
U2 - 10.31083/j.fbl2909322
DO - 10.31083/j.fbl2909322
M3 - Review article
C2 - 39344324
SN - 2768-6701
VL - 29
SP - 1
EP - 12
JO - Frontiers in Bioscience - Landmark
JF - Frontiers in Bioscience - Landmark
IS - 9
M1 - 322
ER -