Tauopathy is a hallmark of a broad category of neurodegenerative conditions and Traumatic Brain Injury (TBI). Progression of tau pathology may lead to impaired cognitive conditions leading to dementia. However, previous studies have reported cognitively healthy patients with cortical tau pathologies. The mechanism for this cognitive protection in a tauopathy environment is being investigated by various groups. Astrocytes are essential for physiological homeostasis of brain and reactive astrogliosis is an associated pathology in neuroinflammation associated with TBI. The correlation between levels of cortical astrogliosis and dementia status of TBI patients at similar tau pathology staging is an unanswered problem. In our investigation we addressed this question by studying hippocampal and parietal cortex tissues from a subset of open access study patient dataset. In our investigation, the cohort was grouped according to thetauopathy status based on Braak staging analysis and dementia status following trauma. We analysed the astrogliosis and microgliosis using GFAP and IBA1 as marker, respectively. Ourwork identified a significantly lower level of astrogliosis in cohort with early tauopathies and no associated dementia. This was missing in late stage tauopathies with no dementia and also withmicrogliosis. In summary, our analysis hints towards a possible protective role of reduced astrogliosis in dementia associated with tauopathies following TBI.