Salk Institute researcher Marguerite Prior holds a vial of J147, a potential Alzheimer's drug that has reversed symptoms of the disease in mouse studies.



— Salk Institute researchers say they may have found something that has eluded the best brains in medical research for decades: A drug that can not just stop but reverse symptoms of Alzheimer’s disease.


The drug candidate, called J147, reversed memory loss in Alzheimer’s model mice, according to a study published online Monday in the journal Alzheimer’s Research and Therapy. The study builds on earlier research finding that the drug preserves brain function when given to Alzheimer’s model mice. That study was published on December 2011 in the journal PLoS One.



Salk scientists develop drug slowing Alzheimer's


This video from the Salk Institute describes how J147 works



After six years of preclinical studies, J147 is ready for human clinical trials, said Dave Schubert, head of Salk’s cellular neurobiology laboratory. The compound, derived from the curry spice component curcumin, has low toxicity and actually reverses damage in neurons associated with Alzheimer’s, said Schubert, the study’s senior author. The lead author is Marguerite Prior, a research associate in Schubert’s laboratory.


However, a history of failed or disappointing drugs for the brain-destroying disease indicates a steep uphill road. Last week. Baxter International said it would stop late-stage trials of its Alzheimer’s drug Gammaguard, after it failed its main goal of slowing cognitive and functional decline in patients with mild to moderate Alzheimer’s.


And those Alzheimer’s drugs that have reached the market only temporarily relieve symptoms.



Memory improvement with J147


Tests show J147 improves memory in Alzheimer's model mice. Also, how the drug originated with cuisine. Hint: use the curry.



Prior said J147’s ability to reverse cellular damage and low toxicity puts it in a class apart from all other Alzheimer drugs. And the ability to repair neuronal damage may make J147 useful in treating other neurodegenerative diseases, Schubert said.


The study subjected mice to various memoery tests. One test placed mice in a pool with a submerged escape platform. The platform was identifiable by cues they had been exposed to earlier, Prior said. The mice had been treated with the drug scopolamine, causing Alzheimer’s-like memory loss. In another variant, aged transgenic mice with Alzheimer’s-like symptoms were tested in the pool.


In both cases, mice that got J147 “significantly” outperformed mice that didn’t get it, Prior said.


Reversing Alzheimer’s symptoms in people is probably too much to hope for from the drug, said Lary C. Walker, a researcher at the Yerkes National Primate Research Center at Emory University in Atlanta.


“It looks like an interesting compound that will have therapeutic utility, whether in AD or not; they have done a good job of characterizing the pharmacokinetics and safety,” Walker said by email, referring to how the body reacts to the drug.


He cautioned that the Alzheimer’s mice used in the study exhibit differences from the pathology of actual human patients, such as the lack of deposits of tau proteins believed to be a cause.


“Therefore your question about whether it will work in humans is a good one, particularly in the advanced stages when the brain is devastated,” Walker wrote. “I think it is unlikely.”


The paper said that despite the differences in pathology, J147 produces a “quite extensive” range of effects pertinent to treating people. For example, the drug increases the level of molecules called neurotropic factors essential for memory.







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