Traumatic Brain Injury by Weight-Drop Method Causes Transient Amyloid-β Deposition and Acute Cognitive Deficits in Mice

Figure 2

Short-term and long-term effects of traumatic brain injury (TBI) on immunohistochemistry of amyloid precursor protein (APP) accumulation in wild-type (WT) mice. (a, b) Representative photographs demonstrating the axonal immunoreactivity for APP in the hippocampal commissure 7 days after the injury: (a) sham-treated WT mice and (b) TBI-treated WT mice. (c, d) Representative photographs showing the axonal immunoreactivity for APP in the hippocampal commissure 28 days after the injury: (c) sham-treated WT mice and (d) TBI-treated WT mice. Arrowheads represent APP-positive areas in the hippocampus. (e, f) Partial quantification of hippocampal APP accumulation. The presence of APP (expressed as the percentage of the area occupied by APP-immunopositive deposition in the ipsilateral hippocampus) was assessed. The region of CA1 used for APP quantification was outlined by a white line in (a). APP accumulation was significantly greater in the TBI-treated WT (closed bar) mouse hippocampus both 7 days and 28 days after injury. and when compared with sham-treated WT mice (open bar). Scale bar, 200 μm.