Age-at-Injury Determines the Extent of Long-Term Neuropathology and Microgliosis After a Diffuse Brain Injury in Male Rats

Traumatic brain injury (TBI) can occur at any age, from youth to the elderly, and its contribution age-related neuropathology remains unknown. Few studies have investigated relationship between age-at-injury pathophysiology a discrete biological age. In this study, we report immunohistochemical analysis of naïve rat brains compared those subjected diffuse TBI by midline fluid percussion (mFPI) post-natal day (PND) 17, PND35, 2-, 4-, or 6-months All were collected when rats 10-months age ( n = 6–7/group). Generalized linear mixed models fitted analyze binomial proportion count data with R Studio. Amyloid precursor protein (APP) neurofilament (SMI34, SMI32) neuronal pathology counted in corpus callosum (CC) primary sensory barrel field (S1BF). Phosphorylated TAR DNA-binding 43 (pTDP-43) was S1BF hippocampus. There significantly greater extent APP SMI34 axonal pTDP-43 following naïves regardless region age-at-injury. However, did determine dendritic (SMI32) CC where all brain-injured exhibited naïve. No significant differences detected astrocyte activation rats. Microglia counts conducted S1BF, hippocampus, ventral posteromedial (VPM) nucleus, zona incerta, posterior hypothalamic nucleus. deramified microglia, whether recent remote, but only occurred The microglia colocalized CD68 TREM2 naïve, remote. Only CD68-positive naive hippocampus Whilst, remote brain-injury displayed Thus, chronic alterations microglial characteristics are evident injured despite recency injury.