In a small laboratory study on mice, Israeli researchers believe they have found a cure for Alzheimer’s, utilizing a molecule they manufactured that alters the “engine” in cells that reduce brain function. The scientists are optimistic about how the synthetic drug can help human patients but say it will take several more years before it could become available on the pharmaceutical market.
Neuroscientists at Ben Gurion University treated 30 mice suffering from Alzheimer’s disease with the special molecule. The results were remarkable. All the mice recovered their full cognitive abilities. The research was peer-reviewed, and the report was recently published in the Translational Neurodegeneration journal.
Most treatments for Alzheimer’s are aimed at reducing the build-up of plaque in the brain (protein build-up between nerve cells). The team from Ben Gurion focused instead on a different aspect of dysfunction for Alzheimer patients—the mitochondria in the brain. Mitochondria are the fuel cells or “engine” in our cells. In Alzheimer’s patients, the mitochondria slow down, and the cells start to die, leading to inflammation and a suppressed immune response.
“We are taking a very different approach than efforts at Alzheimer’s medicines that we have seen so far,” said the lead author of the study, Prof. Varda Shoshan-Barmatz. “Most are trying to address plaque that forms in the brain, but we are addressing dysfunction elsewhere. And we’re optimistic. Mice who had Alzheimer’s and received our molecule and then underwent tests had the same cognitive abilities as mice who’d never had Alzheimer’s.”
Researchers also noted that the mitochondria molecule was effective, even though the plaque levels in the mice were not significantly reduced.
The molecule developed by the Ben Gurion team addresses a malfunction in a protein called VDAC1. This protein plays a vital part in regulating the metabolic energy of mitochondria. In Alzheimer’s, the protein is over-produced, which leads to the cell “burning out,” basically.
“We prevent this protein from causing cell death, as the molecule interferes with its harmful effect,” said Shoshan-Barmatz.
The Ben Gurion team’s research unearthed the components needed to form a molecule that binds to the VDAC1 protein. This molecule was given to 30 mice. While another group of mice with Alzheimer’s did not receive the treatment.
“By binding to the VDAC1, it prevents it from causing neuronal cell death and other changes associated with Alzheimer’s, including neuro-inflammation and neuro-metabolic dysfunctions,” Shoshan-Barmatz said. “The mice underwent various tests. At the start, they had loss of memory and impaired cognitive ability. But by the end of the experiment, the mice who received the molecule had the same memory and cognitive ability as mice without Alzheimer’s.”
“Almost no cell death exists in healthy mice. In the mice with Alzheimer’s, there was a massive neuronal cell death. The molecule prevented neuronal cell death and thus other changes associated with Alzheimer’s, including neuroinflammation and neuro-metabolic dysfunctions. The effects were reflected in the prevention of the decline of cognitive skills such as learning and memory in the sick mice,” she said.
Prof. Shoshan-Barmatz said they have created a company called Tamarix that they hope will be able to bring the treatment to market within seven to ten years.
