An epidemiological association between traumatic brain injury (TBI) and Alzheimer's disease (AD) has long been established. Interestingly, an increase in beta amyloid (one hallmark of AD) directly following TBI has been observed. In fact, it has been reported that with a greater level of TBI comes a higher risk of developing AD, or other neurodegenerative disorders, in the future. Roberts et al first presented research that beta amyloid plaques found in TBI patients are very similar to those found in AD patients. Amyloid precursor protein (APP) is a transmembrane protein that has high expression levels in the brain. In the nonamyloidogenic pathway, APP is cleaved by gamma and beta secretases, which can produce amyloid beta fragments. These amyloid beta fragments become misbalanced in the brain, which contributes to how amyloid beta is produced and regulated. In order to better understand this cellular behavior, various pathways, receptors, and enzymes have been investigated in order to unravel molecular mechanisms. The use of a beta amyloid antibody (MOAB-2) in neuroscience research has served as a useful diagnostic tool.
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Immunohistochemistry: beta Amyloid Antibody (MOAB-2) [NBP2-13075] - IHC analysis of beta Amyloid on normal mouse brain (left) and 5xFAD mouse brain (right) using DAB with hematoxylin counterstain. The MOAB-2 antibody was used at 1:20 on normal mouse brain and at 1:400 on 5xFAD mouse brain.
Collins et al used a beta amyloid antibody (MOAB-2) in their study of focal brain injury on beta amyloid plaque deposition, inflammation, and synapses in an APP mouse model of AD. Focal injury was induced in 3 and 9-month old APP/PS1 and wild-type mice by insertion of a needle into the somatosensory cortex and monitored 1d and 7d post injury. A beta amyloid antibody (MOAB-2) was used in immunofluorescence on 3 and 9-month old rat tissue samples and it was determined that focal injury did not induce MOAB-2 labeled plaques at either time point. Additionally, a beta amyloid antibody (MOAB-2) was used in immunofluorescence to show that while cortical amyloid beta plaques were present in the nine-month-old APP mice, there was no indication of MOAB-2 labeled amyloid beta plaques surrounding the injury site. All in all, it was concluded that APP/PS1 mice recover lost synaptophysin expression even in the presence of amyloid beta plaques.
Yu Yu-Wen et al also used a beta amyloid antibody (MOAB-2) in their research of glucose dependent insulinotropic polypeptide (GIP) and its effects on traumatic brain injury and neuroinflammation in rats. Due to previous research suggesting that neuroinflammation leads to reactive astrocytes, which can lead to APP formation and amyloid beta plaque degradation, Yu Yu-Wen et al used a beta amyloid antibody (MOAB-2) in western blot to investigate the potential neuroprotective behavior of GIP. The results of this experiment showed an elevation of amyloid beta (among BMX and GFAP) following mild traumatic brain injury (TBI) in rats without GIP treatment. Overall, this suggests that GIP has possible rescuing effects on mild TBI related special memory loss and other memory impairments over time.
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