Metallostasis in Alzheimer's disease —Ayton 2013

This is an audio summary of the article "Metallostasis in Alzheimer's disease" by Ayton in 2013. Multiple large-scale clinical studies for Alzheimer's disease (AD) have again failed to achieve their clinical goals in 2012. The onus is now on AD researchers to look at other solutions to achieve outcomes for patients, since the societal and financial cost of this illness grows yearly. Three minor clinical trials focusing on metal interactions with A have all had positive results for patients, despite the failure of numerous significant clinical trials targeting A. Here, we examine the supporting data for the metal theory of AD, including genetic, clinical, biochemical, and pharmacological evidence. The AD-affected brain experiences metallostasis, or exhaustion from metal trafficking, which causes metals to be redistributed into the wrong compartments. Iron, copper, and zinc make up the trio of transition elements that form the foundation of the metal hypothesis. The hypothesis has developed since initial studies revealed the amyloidogenic and oxidative stress effects of these metals; more recently, disease-related proteins, including APP, tau, and presenilin, have been shown to have significant roles in metal regulation, shedding light on the neurodegeneration process in AD and opening up new therapeutic possibilities. This is the end of this informational audio track on "Metallostasis in Alzheimer's disease" by Ayton.

Metallostasis in Alzheimer’s disease. (2012, November 8). Metallostasis in Alzheimer’s Disease - ScienceDirect. https://doi.org/10.1016/j.freeradbiomed.2012.10.558