Tau oligomers from traumatic brain injury (TBI) were associated with accelerated cognitive decline and pathologic seeding in a mouse model, suggesting the importance of their role in TBI. “Scientists have identified altered, dysfunctional tau as a factor in the memory loss and other symptoms associated with both Alzheimer’s disease and TBI. These results suggest that the increased risk for development of neurodegenerative diseases later in life after TBI may be dependent on the presence of toxic tau. Tau oligomers therefore may represent a good target for the prevention and treatment of these disorders,” wrote Rakez Kayed, PhD.
Dr Kayed and colleagues isolated the protein from a mouse model with induced TBI in order to understand the impact of the tau oligomers. They injected purified tau oligomers into the brains of cognitively normal mice to observe the pathology and development of cognitive impairment. Mice with blast-induced TBI were found to have high levels of tau oligomers in the hippocampus, with significantly higher levels observed with immunofluorescent staining (P=.0217). Further, cognitively normal mice with hippocampal injections of tau oligomers performed significantly worse on spontaneous alternation for a spatial memory task (P=.0091). Likewise, mice with hippocampal injections of tau oligomer were found to have increased levels within the cerebellum, “suggesting that tau oligomers may be responsible for seeding the spread of pathology following TBI.” Neuroblastoma cells treated with isolated tau oligomers demonstrated evidence of less cell viability (P=.0005). Conversely, when isolated tau oligomers were pretreated with a tau oligomer monoclonal antibody, the toxic effects were attenuated and cell viability did not seem to be altered.