Rabbit Anti-Human beta Amyloid monoclonal antibody, clone I42M32

The use of -amyloid precursor protein (-APP) immunocytochemistry is standard practice in forensic neuropathology to assess the presence and severity of traumatic axonal injury. However, axonal injury has many causes, in addition to trauma. The principal complicating factor in interpretation is where traumatic brain injury is associated with brain swelling or hemorrhage, resulting in ischemic axonal injury. Although it has been claimed that different patterns of -APP immunoreactivity are seen in trauma, as opposed to hypoxia-ischemia, there have been few systematic studies of -APP immunostaining patterns in ischemic or hemorrhagic stroke. This study investigated staining patterns in 96 cases of stroke with no history of head injury and found complex staining patterns, some of which were indistinguishable from those said to be specific for trauma. A questioning approach to the assessment of -APP immunostaining patterns in cases of head injury is proposed to ensure that the possibility of some or much of the staining being due to ischemia has been excluded, before concluding that the axonal injury identified is traumatic in causation.

High-mobility group box 1 (HMGB1), a nuclear protein that has endogenous cytokine-like activity, is involved in several neurological diseases by mediating inflammatory response. In this study, a lateral head rotation device was used to establish a rat diffuse axonal injury (DAI) model. The dynamic expression of HMGB1, apoptosis-associated proteins, and proinflammatory cytokines were detected by Western blot, and neuronal apoptosis was observed by TUNEL staining. The extracellular release of HMGB1 and the accumulation of beta-APP were observed by immunofluorescence and immunohistochemistry, respectively. The brain injury was indicated by modified neurological severity score (mNSS), brain water content (BWC), and the extravasation of Evans blue. We showed that HMGB1 level obviously decreased within 48 h after DAI, accompanied by neuronal apoptosis, the activation of caspases 3 and 9, and the phosphorylation of BCL-2. Inhibiting HMGB1 with glycyrrhizic acid (GL) can suppress the activation of apoptosis-associated proteins and inhibit the expression of proinflammatory cytokines, which ameliorated motor and cognitive deficits, reduced neuronal apoptosis, and protected the integrity of blood brain barrier (BBB) and axonal injury after experimental DAI in rats. Thus, HMGB1 may be involved in the inflammatory response after DAI, and inhibition of HMGB1 release with GL can notably alleviate the brain injury after DAI.