Hi there! This is Andy Hims, class of 2021. When Andy had first intended to major in Neuroscience, he was primarily interested in consciousness and how it arose from the cluster of cells and fat in our head. However, as he progressed through college, he obtained a deeper sense of mindfulness and appreciation of the world around him. The beauty of simply existing captivated him, but it also served as the ultimate memento mori and the ultimate motivation to continue studying the sciences. Since then, he has brought unparalleled passion and drive to research how to combat and slow aging.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that causes neuronal loss and characterized to have the histopathological hallmarks of β-amyloid plaques and neurofibrillary tangles. The current hypotheses for the etiology and treatment of AD were deduced from these hallmarks, centering on proteopathic cascade hypotheses such as the β-amyloid cascade hypothesis and the phosphorylated-tau hypothesis. While these hypotheses have been supported with pharmaceuticals targeting these on animal models, all have current drugs have failed to produce the desired result in human clinical trials. Because of this, proteopathic hypotheses have been increasingly questioned and other hypothesis are beginning to appear such as the accelerated aging hypothesis. The accelerated aging hypothesis claims that AD is not unique in its set of contributing factors, rather they are characteristic of neuronal aging, and are found earlier at an accelerated rate in AD. If that is the case, then studying the etiology of AD must begin by studying the hallmarks of aging to see how aging may contribute to neuronal and synaptic loss in AD. By formulating an extensive literature review drawing connection between Alzheimer’s and aging, I come to the conclusion that the accelerated aging hypothesis can serve as a unifying hypothesis, combining elements of the proteopathic hypothesis into a single idea to describe AD. This oral presentation will focus on critiquing the current situation of the proteopathic hypotheses and analyzing how aging may be regarded as a unifying hypothesis for AD.