Enzyme Experiment in Mice Has Reversed Their Alzheimer’s

Enzyme Experiment in Mice Has Reversed Their Alzheimer’s

By Diana Rodriguez

Alzheimer’s is a neurodegenerative disease that affects over 5.5 million Americans, with symptoms ranging from short term memory loss to not being able to remember the past 40 years of one’s life.

The enzyme beta-secretase (BACE1) encodes a protein that is the main ingredient in amyloid plaque buildup between nerves in the brain, cutting off communication, and causing the Alzheimer’s.

Recently, an experiment showed that brain plaque associated with Alzheimer’s quickly disappeared when researchers deprived mice of BACE1. Scientists presiding over the experiment hypothesized that stopping the production of the enzyme would slow or stop the plaque from growing, but it did even better: existing plaque began to vanish.

The researcher at the forefront of this experiment, Riqiang Yan, is vice chair of neuroscience at the Cleveland Clinic Lerner Research Institute. He says that four different drugs targeting BACE1 are already being tested, but advises caution, as BACE1 is essential for other neural functions.

As such, inhibiting the mice of this enzyme comes with its share of cons. The mice in the experiment were observed to have experienced hyperactivity, abnormal astrogenesis (production of star-shaped cells in the brain), impaired pathfinding, and long-term depression.

Given these drawbacks, the next step towards possibly curing the disease seems to be conducting the same experiments on animals more similar to humansin this case, rats.

Episodic memory—a form of memory that refers to the recalling of events, including the time, place, people involved, and associated emotionsis one of the first things to disappear with Alzheimer’s. Until recently, it had only been researched and found in chimpanzees, gorillas, and scrub jays.

Jonathan Crystal, head of the neuroscience department at Indiana University, conducted an experiment with his team that supported their suspicions that rats had episodic memory, thus making them great candidates for Alzheimer’s experiments.

Unfortunately, though 2012 was a big year for experimental Alzheimer’s medications, the drugs created that worked for animals did not fight the disease in humans. This is thought to be because despite certain similarities, our cognitive systems are just not enough alike.

Because of this, scientists are now perfecting transgenic micewhich have human genes artificially transferred into their systemsso that their memories can be more like those of humans. The field is expected to hold some promising advancements towards the eradication of such a common, debilitating disease as Alzheimer’s.

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