Abstract
Abstract: There is no question as to whether or not the beta amyloid (Aβ) peptide plays a role in the exacerbation and onset of AD. There are very evident correlations between the volume of Aβ deposition in the AD brain and the severity of the symptoms of AD-typical neurodegeneration. There are certainly many factors involved in the progression of AD, of which the aggregation of Aβ peptides is only one. While many have ruminated on the mechanism by which Aβ serves to impair synaptic function and contribute to neurodegeneration, the role of this protein has yet to be fully uncovered, not just in the AD brain, but in the normally functioning brain as well. Recent research has shed light on the role of Aβ in the normal brain, offering evidence for the fact that beta amyloid functions as an antimicrobial protein, with its primary objective being to serve an immunoresponsive purpose. This text will highlight some of the critical studies on the topic, and illuminate the role that Aβ most likely plays in the functioning of the normal brain, and how this influences its pathological deposition in the AD brain.
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