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Oklahoma City doctor making stunning strides in reversing Alzheimer’s effects

Intricate models are just one of many effective tools used by famed Alzheimer’s researcher Dr. Jordan Tang. of the Oklahoma Medical Research Foundation. Models replicate the inner workings of the human body. Tang recently collaborated on another major Alzheimer’s discovery. Photo provided.

Note: This is another installment in multi-story package on senior citizen issues investigated by Editor Stacy Martin.

Famed Oklahoma City Alzheimer’s researcher Dr. Jordan Tang and a Purdue scientist have made a stunning step forward in reversing the effects of Alzheimer’s in mice, indicating human trials are not far off, said Oklahoma Medical Research Foundation officials.

However the news is tempered by the fact that the Food and Drug Administration (FDA) requires several years of tests and examination to assure the drug’s safety. Additionally, it is one of most promising compounds developed thus far, OMRF officials said.

“Alzheimer’s is a complicated, multi-faceted disease, so it’s important to press forward on as many fronts as possible” said Tang, who holds the J.G. Puterbaugh Chair in Medical Research at Oklahoma Medical Research Foundation. “We cannot rely on a ‘one-treatment-fits-all’ strategy, because what works in one patient will not necessarily work in another.”

Although officials were reluctant to pin down a possible alzheimer’s drug availability to the public, the development is still another big leap forward, said Dr. Stephen Prescott, OMRF President Dr. Stephen Prescott..

“It’s a major advance,” said Prescott. “The really dramatic event is this compound is such ore potent than some developed in the past.”Now we have to test more extensively in animals for safety. And we are optimistic that it will (be safe).

Then, there’s a very rigorous regulatory process ahead and we would not be in charge of the timeline. But it’s realistic to think it could be in human testing in a couple of years.”

Prescott said there was some disappointment a few weeks ago that some compounds already developed were only successful on a limited basis. The new discovery has much stronger effects and thus, more broad application potential.

In this latest discovery, OMRF scientists developed an experimental compound that reduces memory loss and Alzheimer’s disease-causing plaques in mice that are genetically engineered to develop the illness.

The animals were treated with a new compound developed by a team led by OMRF’s Jordan Tang, Ph.D., and Purdue University’s Arun Ghosh, Ph.D. “With treatment, we found a reduction in disease-causing plaques of 75 percent,” said Tang. “And the mice performed almost as well in memory tests as mice without the Alzheimer’s gene.”

Based on these results, the researchers will continue to study and develop the compound as a possible treatment for Alzheimer’s in humans.

An experimental drug based on Tang and Ghosh’s previous work is already undergoing trials in humans, but the latest research involves a new and different compound formulated by the OMRF team.

The new compound inhibits an enzyme known as memapsin 2. “Memapsin 2 is like a pair of biological scissors in the brain, snipping off sections of a chain of amino acids,” said Tang. “As we get older, those snipped strands become tangled together and form plaques that cause Alzheimer’s disease.”

OMRF technicians gave regular doses of the new inhibiting compound to laboratory mice genetically engineered to develop a condition similar to Alzheimer’s. They then compared the brains of the mice to genetically altered mice that did not receive the inhibitor. By the age of 10 months, the brains of untreated mice showed the same plaques found in humans with Alzheimer’s, but mice given the inhibitor showed only a fraction of those plaques.

The researchers also administered a memory test for the mice by submerging a platform beneath a pool of opaque liquid and allowing the mice to swim around to find it. They then repeated the test several times to assess the animals’ ability to remember the platform’s location. The better a mouse’s memory, the faster the animal was able to find the platform.

The mice that received the inhibitor were able to remember the location of the platform almost as well as normal mice. In contrast, mice with the Alzheimer’s genes that did not receive the inhibitor began to experience difficulty finding the platform at around 6 months, and their performance continued to decline as they aged.

The research appears in the new issue of The Journal of the Federation of American Societies for Experimental Biology. In addition to Tang, three other OMRF researchers were co-authors of the study: Wan-Pin Chang, Ph.D., Xiangping Huang, Ph.D., and Deborah Downs. The National Institute on Aging funded the work.

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