ABSTRACT
Traumatic brain injury (TBI) may be encountered in any sport and is considered an important public health concern. In view of the clinical data suggesting a possible genetic influence on neurological outcome after TBI, further understanding of the physiological functions of Apolipoprotein E is necessary. TBI in sports has the propensity to be associated with significant morbidity and possible mortality. Accordingly, identifying potential risk factors for TBI in sports is of paramount importance. Amyloid deposition is a potentially important neuropathological consequence associated with TBI. Evidence of axonal injury has also been documented in milder forms of TBI. Animal studies suggest that cholinergic neurotransmission may be selectively vulnerable to the effects of TBI and that this disruption is partially responsible for the cognitive impairment associated with TBI. Human studies have provided additional evidence of altered cholinergic transmission following TBI.
