The+Role+of+Autophagy+in+Alzheimer's+Disease


 * The Role of Autophagy in Alzheimer’s **

Autophagy ensures the synthesis, degradation and recycling of cellular components. To do this, organelles and cytosol are engulfed into an autophagosome which fuses with a lysosome. The lysosome contains acid hydrolases which breakdown the cellular components. Autophagy was discovered by Christian de Duve in 1949 by studying the effects of insulin on liver cells. = = = Figure 1. Basic pathway of autophagy to breakdown cellular components. =

= = ==== Alzheimer’s is a neurodegenerative disease typically found in the elderly. It is believed that by the age of 85, 50% of humans will have developed Alzheimer's disease. Symptoms include a loss of memory and an overall cognitive decline. Alzheimer’s is characterized by the brain containing an abundance of amyloid plaque aggregates. These plaques are normally hindered from forming because autophagy is responsible for digesting the beta-amyloid protein which forms the plaques. When autophagy is inhibited, or slows down as humans grow older, these plaques begin to aggregate in the brain and are toxic to the cells surrounding, in effect, killing them. ====

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The role of autophagy on Alzheimers is demonstrated in a study, "//Aβ Secretion and Plaque Formation Depend on Autophagy" //in which mice with genetic variations, caused them to produce beta-amyloid protein in excess and also exhibit hindered autophagy. It was found that the beta-amyloid accumulated inside of the cell due to the mice not being able to perform autophagy efficiently. This caused the mice to exhibit the physical signs of Alzheimer's, such as confusion and memory loss. ===== = Bibliography: =

====// **Aβ Secretion and Plaque Formation Depend on Autophagy ** //**(Per Nilsson //et al.).//** ====

====This paper studied mice with a genetic variation that causes them to produce additional beta-amyloid proteins and have inhibited autophagy. This was done to induce early-onset Alzheimer’s Disease. The researchers studied the amounts of Beta-amyloid plaque that developed inside and outside the cell. Their results showed an increase in the amount of plaque inside brain cells compared to healthy mice. They concluded that this was due to autophagy failing to successfully remove the plaque. ====

** //Cell ‘‘Self-Eating’’ (Autophagy) Mechanism in Alzheimer’s Disease// (Sarah Funderburk //et al.//) **
==== This is a review article that describes in great detail different models and theories that may attribute to the development of Alzheimer’s due to deficient autophagy. ====

====** //Reversal of autophagy dysfunction in the TgCRND8 mouse model of Alzheimer's disease ameliorates amyloid pathologies and memory deficits //(Dun-Sheng Yang //et al.//) **==== ==== This study did something somewhat different than the others. The authors attempted to increase the rate of autophagy in mice with higher beta-amyloid plaques. They discovered that restoring autophagy in autophagy-deficient mice led to decreasing amount of accumulated beta-amyloid proteins. ====