Oct 17, 2016 12:53 AM EDT By Chris Brandt, UniversityHerald Reporter

Forgive the pun but Alzheimer's disease might soon be a forgotten memory with the new breakthrough made by a team of scientists from the University of Minnesota. The team was able to reverse the effect of Alzheimer's in lab mice after they discovered a specific enzyme believed to be the culprit in this debilitating disease.

The team, headed by Dr. Karen Ashe, a neurology professor at the University of Minnesota, have been studying the disease for 10 years in hopes to find out what disrupts the brain of those who have Alzheimer's disease.

The research paid off after they have discovered a specific enzyme, Caspase-2, which attacks the brain neurons and targeting a specific protein in the brain called tau. By focusing on the process, they were able to reverse the process and restore memory deficits.

Dr Ashe said that a lot of studies have been made about this devastating disease but a lot have focused on the "accumulation of tangles and their connection to memory loss." After years of study, however, they begin to discover that these tangles are the less likely the cause of the disease.

"The pathological fragment of tau that we have identified resists forming tangles and can instead move freely throughout the cell," Ashe said, "Therefore, we decided to look for other mechanisms that could affect synaptic function."

To prove if their theory was correct, the team used fluorescent labeling in order to fully observe the behavior of normal and mutated tau in the mice hippocampus, the area of the brain associated with memory and learning.

Mutated tau together with the short fragment produced when the caspase-2 enzyme cuts the tau are mainly found in the dendritic spines, which acts like the receiving area for neurons when neighboring cells send a message. Overabundance of these two elements in the spines disrupt its synaptic functions.

The scientists also made this very significant discovery: the mutated taus are disrupting the ability of neurons to properly receive and respond to signals causing "memory deficits independent of tangle formation."

In layman's terms, there is no cell death or synapses loss when this process happens. With this discovery, there is a better chance of reversing the symptoms and stopping the process said Dr. Ashe.

The study, which was funded by the National Institutes of Health's National Institute of Neurological Disorders and Stroke, is published in the Nature Medicine journal.

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