Traumatic brain injury (TBI) is one of the leading causes of long-lasting morbidity and mortality worldwide, being a devastating condition related to the impairment of the nervous system after an external traumatic event resulting in transitory or permanent functional disability, with a significant burden to the healthcare system. Harmful events underlying TBI can be classified into two sequential stages, primary and secondary, which are both associated with breakdown of the tissue homeostasis due to impairment of the blood-brain barrier, osmotic imbalance, inflammatory processes, oxidative stress, excitotoxicity, and apoptotic cell death, ultimately resulting in a loss of tissue functionality. The present study provides an updated review concerning the roles of brain edema, inflammation, excitotoxicity, and oxidative stress on brain changes resulting from a TBI.
View Article and Find Full Text PDFBackground: Neural cells undergo functional or sensory loss due to neurological disorders. In addition to environmental or genetic factors, oxidative stress is a major contributor to neurodegeneration. In this context, there has been a growing interest in investigating the effects of EOs (EOs) in recent years, especially in the treatment of neuropathologies.
View Article and Find Full Text PDFSenescence is a physiological and progressive event that leads to the impairment of normal functions of the organism. The nervous system is one of the most affected systems during aging, presenting both structural and functional alterations associated with a decline in normal brain functions. In the present study we aimed to evaluate the impact of senescence on the mesolimbic pathway (nucleus accumbens - NAc and ventral tegmental area - VTA) of the rat, through immunohistochemistry for tyrosine hydroxylase (TH) enzyme, in young (3 months old), middle-aged (10 months old) and aged animals (18 months old).
View Article and Find Full Text PDF