Thursday, March 30

The Alzheimer’s vaccine, closer



The finding is due to a team of scientists from the University of Leicester (UK), the University Medical Center Göttingen (Germany) and the research charity LifeArc. In the abstract of the study they allude verbatim to a “Surprising reduction in amyloid plaque formation”, the pathological accumulation of beta-amyloid peptide that causes the neuronal disconnection that characterizes Alzheimer’s.

Other drugs had proven ineffective and even counterproductive in destroying these plaques. This promising new approach uses a dual pathway, an antibody-based treatment and a protein vaccine; and a different target: instead of targeting beta-amyloid plaques, both substances target a different form of this protein. The beta-amyloid peptide exists naturally in our brain and forms rope-like molecules that can accumulate to form fibers or plaques. In Alzheimer’s patients, a high proportion of these proteins are shortened or “truncated”. They are what some scientists consider key in the development of the disease.

Thomas Bayer, from the University Medical Center of Göttingen, notes that their team identified an antibody in mice that neutralized the truncated forms of soluble beta-amyloid, but would not bind to normal forms of beta-amyloid or to plaques. For his part, Dr. Preeti Bakrania and his LifeArc team isolated and adapted the antibody found in mice so that the human immune system would not reject it as a foreign body. This antibody, TAP01_04, proved to be very effective in vaccines and experimental treatments.

Another of the study authors, Professor Mark Carr, from the Institute of Chemical and Structural Biology at the University of Leicester, explains that the modified form of beta-amyloid could potentially be used as a vaccine, to activate a person’s immune system to produce TAP01 04-type antibodies.

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The Göttingen group tried both the “humanized” antibody such as the modified beta-amyloid vaccine – which they gave a very Spanish name, “TAPAS” -, in two different Alzheimer’s models in mice. Drawing on imaging techniques similar to those used to diagnose Alzheimer’s in humans, they found that both the antibody and the vaccine helped restore neuronal function, increase glucose metabolism in the brain, staunch memory loss, and – although not was the goal of the research – to reduce the formation of beta-amyloid plaques.

The scientists, who are looking for a commercial partner to conduct clinical trials of the antibody and the vaccine, acknowledge that the research is at a very early stage. Still, Mark Carr recalls that, if these results were replicated in human clinical trials, “they could be transformative. The possibility opens up not only to treat Alzheimer’s once symptoms are detected, but also to vaccinate against the disease before they appear ”.

Alzheimer’s, which represents the 70% of dementias, it begins to develop decades before symptoms appear, which makes the prospect of a vaccine especially interesting.

Nasal vaccine

That of British and German scientists is not the only Alzheimer’s vaccine under investigation. On Tuesday, it was reported that the first human clinical trial of a nasal vaccine against this disease will begin in the United States next month. This drug uses a substance, the Protollin, made up of proteins from bacteria and that can help the body fight some of the proteins and inflammation that contribute to this ailment.

Brigham and Women’s Hospital in Boston announced that it will recruit 16 people between the ages of 60 and 85 with Alzheimer’s in early and symptomatic phase. The vaccine would work by using an experimental immunomodulator that activates white blood cells in the lymph nodes in the neck. Those cells would travel to the brain to eliminate amyloid plaques and other proteins associated with Alzheimer’s.

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The doctor Tanuja Chitnis, a neurologist at Brigham and Women’s Hospital in Boston, professor at Harvard and principal investigator of the clinical trial, pointed out to the prestigious newspaper “The Boston Globe” that “in the last 20 years, evidence has accumulated that the immune system plays a key role in the elimination of beta-amyloid ”.

Much remains to be investigated, but more and more laboratories are betting on this new Alzheimer’s immune target. Like Biogen, which has approved the monoclonal antibody aducanumab, and Nuravax, which is developing a vaccine. The goal is the same: to get rid of the accumulation of beta-amyloid that disconnects brain neurons.


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