Exacerbation of amyloid beta peptide and Tau protein in the cerebrospinal fluid following Traumatic Brain Injury at Hot Environment Neuroproetction by TiO2 nanowired delivery of cerebrolysin with tau antibodies

摘要

Military personnel are prone to develop Alzheimer's disease (AD) during their lifetime. This is attributed largely due to mild traumatic brain injury, stress, hyperthermia and exposure to nanoparticles or chemical fumes during combat operations. All these conditions could induce breakdown of the blood-brain barrier (BBB) and edema formation. BBB breakdowm will allow plasma amyloid beta protein (A(3P) to enter into the brain parenchyma and lead to slowy developing AD. Clevage of amyloid precursor proetin (APP) leads to tau phosporylation that is toxic to neurons and participate in AD process. In present innovation we demonstrate that concussive head injury (CHI) results in increased AβP and tau proetins in the cerebrosoinal fluid (CSF) of rats. This effect is exacerbated in hot environment (HE). As a result, brain pathology, BBB breakdown and edema formation are also exacerbated after CHI in HE. It appears that TiO2-nanwored delivery of cerebrolysin together with antibodies to tau remarkably reduced AβP and tau concetrations in the CSF and induced neuroprotection. This indicates that nanodelivery of cerebrolysin with tau antibodies has supeior neuroprotective ability in CHI, not reported earlier.