Publication: Molecular mechanisms in the pathogenesis of traumatic brain injury
Authors
Ray, S.K. ; Dixon, C.E. ; Banik, N.L.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Traumatic brain injury (TBI) is a serious
neurodisorder commonly caused by car accidents, sports
related events or violence. Preventive measures are
highly recommended to reduce the risk and number of
TBI cases. The primary injury to the brain initiates a
secondary injury process that spreads via multiple
molecular mechanisms in the pathogenesis of TBI. The
events leading to both neurodegeneration and functional
recovery after TBI are generalized into four categories:
(i) primary injury that disrupts brain tissues; (ii)
secondary injury that causes pathophysiology in the
brain; (iii) inflammatory response that adds to
neurodegeneration; and (iv) repair-regeneration that may
contribute to neuronal repair and regeneration to some
extent following TBI. Destructive multiple mediators of
the secondary injury process ultimately dominate over a
few intrinsic protective measures, leading to activation
of cysteine proteases such as calpain and caspase-3 that
cleave key cellular substrates and cause cell death.
Experimental studies in rodent models of TBI suggest
that treatment with calpain inhibitors (e.g., AK295,
SJA6017) and neurotrophic factors (e.g., NGF, BDNF)
can prevent neuronal death and dysfunction in TBI.
Currently, there is still no precise therapeutic strategy for
the prevention of pathogenesis and neurodegeneration
following TBI in humans. The search continues to
explore new therapeutic targets and development of
promising drugs for the treatment of TBI.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.