Research says 30 mice cured of Alzheimer's using newly developed molecule

Israeli scientists have said that they cured mice of Alzheimer's using a newly developed molecule. The scientists gave an artificial molecule to 30 mice suffering from Alzheimer’s and found all of them recovered, regaining full cognitive abilities. The research, led by neuroscientists from Ben-Gurion University, was published in the Translational Neurodegeneration journal.

Speaking to the Times of Israel on Tuesday (February 21), the lead author of the research Professor Varda Shoshan-Barmatz said “We are taking a very different approach than efforts at Alzheimer’s medicines that we have seen so far.”

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“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,” Professor Barmatz added.

According to the Times of Israel report, the molecule appeared to have been effective without significantly reducing the amount of plaque, which Barmatz thought indicated that scientists might have been overly fixated on the plaque. Despite Alzheimer’s being linked to mitochondrial dysfunction, no drug candidates are currently focused on mitochondria.

The report said that Ben-Gurion University set out to normalise mitochondrial activity by countering the harmful effects that occur when VDAC1-a protein- is over-produced.

According to the research, to address the multiple pathways involved in Alzheimer's disease (AD), neuronal cultures and a 5 × FAD mouse model of AD were treated with VBIT-4. "We addressed multiple topics related to the disease and its molecular mechanisms using immunoblotting, immunofluorescence, q-RT-PCR, 3-D structural analysis and several behavioural tests," it added.

The research suggested that mitochondrial dysfunction with its gatekeeper VDAC1 is a promising target for AD therapeutic intervention, and VBIT-4 is a promising drug candidate for AD treatment.

The VDAC1 plays an important role in regulating the metabolic and energetic functions of mitochondria when produced in normal quantities. However, the scientists found that it is produced in huge levels in the brains of mice with Alzheimer’s, and interferes with mitochondrial activity. On Tuesday, Professor Barmatz told the Times of Israel that in the research, the team shifted the focus of Alzheimer’s treatments from the plaque to this protein, which is produced in the nerve cells around the plaque instead.

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“We prevent this protein from causing cell death, as the molecule interferes with its harmful effect,” she said. Her team developed a molecule that binds to VDAC1.

“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,” Barmatz added.

For making the molecule, her team searched scientific libraries for compounds that had qualities suggesting that it would interact with the protein and inhibit its harmful effects. They developed one of the compounds into the molecule, which is designed to prevent changes in the mitochondria. Thirty mice that were suffering from Alzheimer's were given the molecule dosed via their drinking water for five months. Also, a similar number of mice with the disease did not receive the molecule.

Professor Barmatz said on Tuesday the mice underwent various tests. She added that at the start, the mice had a loss of memory and impaired cognitive ability. However, by the end of the experiment, the ones who received the molecule had the same memory and cognitive ability as mice without Alzheimer's.

Barmatz also said, "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."

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