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

Figure 3

Short-term and long-term effects of traumatic brain injury (TBI) on immunohistochemistry of amyloid-β (Aβ) in wild-type (WT) mice. (a, b) Representative photographs demonstrating the axonal immunoreactivity for Aβ in the hippocampus 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 Aβ in the hippocampus 28 days after the injury: (c) sham-treated WT mice and (d) TBI-treated WT mice. Scale bar, 500 μm. Arrowheads represent Aβ deposits in the hippocampus. (e, f) Partial quantification of the hippocampal Aβ deposition. The presence of Aβ (expressed as the percentage of the area occupied by Aβ-immunopositive deposition in the ipsilateral hippocampus) was assessed. (e) WT mice 7 days after sham (control) operation () or the injury (). (f) WT mice 28 days after sham (control) operation () or the injury (). N.S.: not significant; , when compared with sham-treated WT mice. N.S. scale bar, 500 μm.