Longitudinal changes in the DTI measures, anti- @entity538 expression and levels of serum inflammatory cytokines following mild XXXX .

@entity1 @entity131 @entity550 @entity146 @entity310 @entity1184 @entity538 @entity195 @entity1893 @entity688 @entity130
UNASSIGNED: The majority of @entity1 mild @entity131 (mTBI; 70%) lack radiological evidence of injury, yet may present long term cognitive, and @entity146 . With the hypothesis of evident damaged neural tissue and immunological consequences during acute phase of mTBI, we used closed skull weight-drop TBI model to address @entity1 mTBI condition. Serum cytokines ( @entity310 , @entity688 ) and @entity538 ( @entity538 ) expression were examined at day 0 (control, @entity130 ), 4h, day 1, day 3 and day 5 post injury (PI). Diffusion tensor imaging (DTI) was performed at similar timepoints to identify neuroinflammation translation into imaging abnormalities and monitor injury progression. DTI indices including @entity1893 ( @entity1893 ), radial diffusivity (RD), fractional anisotropy and axial diffusivity values were quantified from @entity550 ( @entity550 ), hippocampus and corpus callosum regions. One way ANOVA showed significant increase in @entity310 at 4h and @entity688 at day 1 PI as compared to control. @entity538 (+) cells were significantly increased at day 3 and day 5 as compared to control in @entity550 . Repeated measures ANOVA revealed significant decreases in @entity1893 , RD values in @entity550 at day 3 and day 5 as compared to day 0. A significant, inverse correlation was observed between cortical @entity1893 (r=-0.74, p=0.01), @entity195 (r=-0.60, p=0.03) and RD (r=-0.72, p=0.01) values with mean @entity538 (+) cells in the cortical region. These findings suggest that mTBI leads to elevated cytokine expression and subsequent @entity1184 of astrocytic processes. The increased numbers of reactive glial cells contribute diffusion restrictions in the CNS leading to reduced @entity1893 and RD values. These findings are in line with the deficits and pathologies associated with clinical mTBI, and support the use of mTBI model to address pathology and therapeutic options.
