beta amyloid

By Michalina Hanzel, PhD

By Jamshed Arslan, Pharm. D., PhD.

By Jamshed Arslan Pharm.D.

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.

Inositol-requiring protein 1/IRE1 alpha (also called Endoplasmic Reticulum to Nucleus Signaling 1/ERN1; predicted mol wt 110 kDa) is a serine-threonine protein kinase/endoribonuclease which plays a highly critical role in unfolded protein response/UPR signaling, a mechanism by which eukaryotic cells sense and deal with ER stress. The latter triggers growth arrest and apoptosis in cells with misfolded proteins.

A major histopathological hallmark of Alzheimer's disease (AD) is the presence of amyloid deposits in the parenchyma of the amygdala, hippocampus, and neocortex. The principal component of amyloid is beta amyloid (AB). The pathologic accumulation of AB in plaques is postulated to result from an imbalance between production and clearance during aging.

Amyloid beta (AB) peptide has a central role in the neurodegeneration of Alzheimer's disease (AD). Immunization of AD transgenic mice with AB_-42 peptide reduces both the spatial memory impairments and AD-like neuropathologic changes.

 Synaptophysin (a presynaptic vesicle protein) is an integral membrane glycoprotein originally isolated from presynaptic vesicles of bovine neurons. Synaptophysin is found in all nerve terminals and synaptophysin measurements have been used to quantify the number of terminals present during neuroanatomical remodeling and neural development (1).

By Eric Neeley