New Hope for an Effective Alzheimer’s Drug

Dear Reviewer,

We are entering a dramatic era in which we are likely to defeat many of our worst diseases, such as cancer, heart disease and even neurological disorders like Parkinson’s.

There is a commonality to those diseases — they are all diseases of aging. Young people, with few exceptions, do not get cancers, do not get heart attacks and do not get Parkinson’s. This suggests our model of attacking specific diseases may not be nearly as efficient as attacking their common core — aging itself.

And Alzheimer’s may be the clue that tells us we’re on the wrong path. Because no matter how we approach the consequences of the disease — those horrible amyloid plaques in our brains — we have been unsuccessful. Hundreds of brilliant drug trials for Alzheimer’s candidates have been abandoned over the last 20 years. Nothing has worked to slow the disease itself. Meanwhile, Alzheimer’s has grown to be the third leading cause of death in the United States.

That fact has sparked a different approach at the Salk Institute for Biological Studies in La Jolla, California. The institute has a worldwide reputation for attracting the best scientists in the world. It focuses on problems of aging, including regenerative medicine (think stem cells), the biology of cancer, the immune system, diabetes, neurological disorders and plant biology. There is nothing quite like it.

Researchers at Salk recently disclosed in the journal Aging that they had developed a promising drug after extensive assays of genes in the brain and examining more than 500 small molecules involved with brain metabolism.

The molecule they landed on, called J147, was developed specifically to attack Alzheimer’s in an entirely different way — by going after its major risk factor: getting older. Mice given J147 have improved memories and a host of other physiological changes, like blood vessels in the brain that don’t leak as much, a common problem in aging brains.

Three sets of mice genetically engineered to age rapidly were used: young mice, old mice and old mice fed J147. The old mice fed J147 performed better in memory and cognition tests and had fewer pathological expressions of Alzheimer’s in their brains. They seemed far more like the young mice control group and showed increased energy, less inflammation in the brain and fewer oxidized fatty acids in the brain.

Perhaps most importantly, the large amount of data collected on the three groups of mice showed that many aspects of gene expression and metabolism in the old mice fed J147 were very similar to those of the young animals.

The researchers are eager to begin human trials of J147 next year.

To your health and wealth,

Stephen Petranek

Stephen Petranek

The Daily Reckoning