Neurochemical Profile of Dementia Pugilistica
Year: 2012
Type: article
Abstract: Dementia pugilistica (DP), a suite of neuropathological and cognitive function declines after chronic traumatic brain injury (TBI), is present in approximately 20% of retired boxers. Epidemiological studies indicate TBI is a risk factor for neurodegenerative disorders including Alzheimer disease (AD) and Parkinson disease (PD). Some biochemical alterations observed in AD and PD may be recapitulated in DP and other TBI persons. In this report, we investigate long-term biochemical changes in the brains of former boxers with neuropathologically confirmed DP. Our experiments revealed biochemical and cellular alterations in DP that are complementary to and extend information already provided by histological methods. ELISA and one-dimensional and two dimensional Western blot techniques revealed differential expression of select molecules between three patients with DP and three age-matched non-demented control (NDC) persons without a history of TBI. Structural changes such as disturbances in the expression and processing of glial fibrillary acidic protein, tau, and α-synuclein were evident. The levels of the Aβ-degrading enzyme neprilysin were reduced in the patients with DP. Amyloid-β levels were elevated in the DP participant with the concomitant diagnosis of AD. In addition, the levels of brain-derived neurotrophic factor and the axonal transport proteins kinesin and dynein were substantially decreased in DP relative to NDC participants. Traumatic brain injury is a risk factor for dementia development, and our findings are consistent with permanent structural and functional damage in the cerebral cortex and white matter of boxers. Understanding the precise threshold of damage needed for the induction of pathology in DP and TBI is vital.
Source: Journal of Neurotrauma
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: G1052080286, G1185609304, G1606131442, G2161113364, G250893170, G2898431357, APP/AB/Tau biochemistry in transgenic mice, familial and sporadic AD, G3250808129, G3521153818, G4791902628, G4938771083, G5761650749, G5781525924, G6030318873, G6125194395, Arizona Alzheimer's Disease Core Center, G7125474156, G7161884846, Boston University Alzheimer's Disease Center, Massachusetts Alzheimer's Disease Research Center, G7747731141, G7814413666, G7887587830, G961669115
OpenAlex ID: W1989378970