The Effect of Glial Tau Expression and Traumatic Brain Injury on Heat Shock Protein Expression
Date
2025-07-09
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Abstract
Recent studies examining the brains of footballers and boxers have shown that successive, low-impact traumatic injuries to the head lead to Chronic Traumatic Encephalopathy (CTE), a tauopathy characterized by the aggregation of misfolded Tau both in neuronal and glial cells. Glial cells play a crucial role in overall brain health, but the effect of glial Tau aggregation in CTE, as in other tauopathies, remains unclear. In this project, we used a Drosophila model of human glial tauopathy to investigate the effect of both glial Tau expression and Traumatic Brain Injury (TBI) on the expression of two Heat Shock Proteins (Hsps). Hsps are a class of molecular chaperones that prevent the aggregation of misfolded proteins, and the formation of Tau tangles suggests a deficit in this chaperone system. We have found that Hsp23 and Hsp70 levels attenuate with aging. Moreover, the presence of glial Tau in 3-day-old flies similarly results in a decline in Hsp levels. TBI also leads to a reduction in Hsp70 levels in young flies that do not express glial Tau, while Hsp levels in older flies were resistant to TBI-induced changes. Our results indicate that the Hsp chaperone system is indeed affected by TBI and compromised in tauopathies; the Hsp chaperone system represents a pathological pathway that may be targeted in an attempt to combat tauopathies.
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tau, traumatic brain injury, glia