Possible Alzheimer’s drug also slows aging

SAN DIEGO, California: A potential Alzheimer’s drug works by reducing the rate of aging at the molecular level, according to a new study by Salk Institute scientists.

The study explains how the drug both improves cognition and reduces the rate of aging, when given to very old mice.

Study authors say a drug that inhibits aging may succeed where drugs specifically aimed at Alzheimer’s have failed.

Getting the drug into human clinical trials will require a little over $1 million.

A potential Alzheimer’s drug works by reducing the rate of aging at the molecular level, according to a new study led by Salk Institute scientists.

The study provides an explanation for previously observed signs of improved cognition and rejuvenation, when the drug was given to very old mice.

It found that the drug, called J147, protects the cell’s energy factories, called mitochondria. Brain cells consume enormous amounts of energy, about 25 percent of all energy used in the human body. And mitochondrial dysfunction has been implicated in Alzheimer’s as well as aging-associated deterioration.

Knowledge of the drug target and how it works may help persuade drug companies and investors to fund human studies of the drug, said the study’s senior author, Dave Schubert.

Moreover, a relatively small amount of money will be needed to start human trials, Schubert said. About $150,000 is needed to complete a Food and Drug Administration application to begin trials, with about $1 million more to actually start human testing. An additional $9 million phase of testing, which focuses on safety and memory enhancement, Schubert said.

The study was published in the journal Aging Cell.

Despite billions of dollars spent on Alzheimer’s drugs, results have been disappointing. Drugs on the market temporarily halt the decline in cognition in Alzheimer’s patients. No approved drugs affect the underlying course of the disease.

Schubert and colleagues say it’s time for a new approach to Alzheimer’s drug discovery, based on rolling back the effects of aging, the biggest risk factor for the disease.

Up until very recently, a frontal attack on aging has been considered out of the mainstream, Schubert said. The pharmaceutical industry hasn’t been interested in anti- aging drugs, since aging is considered a natural process, not a disease.

“I was told for the last 10 years not to talk about aging to any pharma or VC people,” Schubert said.

But the repeated failures with Alzheimer’s drugs, most of which of the disease, means it’s time to rethink the strategy, Schubert said.

“People are starting to realize that aging is a viable drug target, and demonstration of that fact,” he said.

For example, the diabetes drug metformin is now being studied as a drug that promotes healthy aging. Schubert said J147 works like met

J147 was developed by exploring the chemical properties of curcumin, an ingredient in the curry spice turmeric. Schubert and colleagues made more than 300 derivatives of curcumin, and screened for their ability to protect the aging brain. Of them, J147 performed the best.

“We are trying all possible avenues to move J147 toward the clinic,” Schubert said.

The study and researchers were funded by grants from the National Institutes of Health, California Institute of Regenerative Medicine, the Nomis Foundation, the Della Thome Foundation; the Bundy Foundation, the Hewitt Foundation, the Paul F. Glenn Center for Aging Research at the Salk Institute, and the Waitt Foundation.