Topic: controlled cortical impact

Traumatic brain injury (TBI) can cause life-changing neurological deficits. There are currently no neuroprotective treatments in TBI. The high content of oxidation-sensitive polyunsaturated fatty acids (PUFAs) in the brain generates an environment vulnerable to TBI-related oxidative damage. We hypothesised that partial replacement of tissue PUFAs with deuterium - enriched PUFAs (D-PUFAs), could act as a brake against oxidation and improve outcome.A moderately severe TBI was induced using a controlled cortical impact (CCI) in adult male and female CD1 mice. Animals received a control or a D-PUF

Acquired brain injuries (ABIs), such as stroke and traumatic brain injury (TBI), represent global health challenges, stroke ranking as the third leading combined cause of death and disability, and TBI contributing to over 7 million disability-adjusted life years. Functional recovery in ABIs is influenced by age, older individuals showing poorer recovery. Axonal plasticity, a form of structural neuroplasticity, holds promise for understanding and promoting recovery. Injuries were carried out in 14-month-old male Wistar rats. Focal stroke was induced by unilateral intracerebral administration of

Aims: Post-injury physical exercise can reduce memory deficits associated to traumatic brain injury (TBI) in late adolescent and young adult rats, but both the effectiveness of this treatment and possible sex-dependent effects in late middle-aged injured rats are important issues still unsolved. The aim of the present work was to examine whether chronic object recognition memory (ORM) deficits associated to TBI can be alleviated by post-injury physical exercise in males and females late middle-aged rats. Methods: 14 months-old rats were submitted to a controlled cortical impact injury model of