Alzheimer’s disease is considered to be the disease that, due to its diffusion and impact on the lives of patients and their families, will weigh on health systems more than any other in a few years from now. Especially since, to date, there are very few tools to combat it. But things are changing: the first drug has been approved in the US and others are being studied. The latest news on their effectiveness comes from the main international congress on this disease – the Clinical Trials on Alzheimer’s Disease (CTAD) Conference – which is taking place these days in Boston.
Alzheimer’s, between classic drugs and new strategies
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The first results arrive on the front of aportanumab, the molecule to which the FDA has granted an accelerated authorization that has sparked several controversies, and concerns the action on the Tau protein, one of the two substances that today are hypothesized to be related to the development and progression of the disease. For years the scientific community was rather divided between those who thought that the accumulations of beta-amyloid protein were driving the process towards degeneration and those who instead pointed the finger at the Tau. “Today it is clear that both are essential for the development of the disease but that the first to accumulate is beta-amyloid which in turn favors the accumulation of Tau”, he explains. Alessandro Padovani, director of the Neurological Clinic, University of Brescia. “In the future we can therefore think of treating the disease by hitting both targets, as we do for many other diseases of which we know different causes”.
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That the two proteins are bound to each other is also evident on the basis of the latest aducanumab data: although its mechanism of action is directed against the accumulation of beta-amyloid, the results presented in Boston show a reduction in levels of Tau. “This is very important because it confirms that aducanumab not only acts on beta-amyloid but also on the phosphorylated version of the Tau protein which is associated with neuron degeneration, and then that this biological effect can be monitored in plasma”. The results derive from the samples conducted on over 1800 patients involved in clinical studies and show that the lowering of Tau levels are associated with a lower cognitive and functional decline measured through four different evaluation scales. An important fact because the correlation between protein levels and cognitive and motor decline appears to be the weak point of the drugs under study.
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“However, we must change perspective: we cannot presume to stop in 18-24 months – this is the length of trials to date – what has accumulated for years and years. We do not ask for this to drugs that act on cholesterol for decrease the risk of heart attack, for example “, explains Padovani. Rather, according to the researcher, we need to figure out whether the drug can slow down the drifting Alzheimer’s ship. He can? “The data tells us yes, but also that it takes time to get rid of all the accumulated amyloid,” says the neurologist.
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Neurologists have known for some time that the road to developing effective Alzheimer’s drugs is a long and winding one. “But we are confident, also in light of these and other data that were presented in Boston by companies that pursue both paths”, concludes Padovani. Like those on semorinemab, a molecule not yet authorized, which targets Tau, preventing its aggregation. The data presented in Boston show that this approach, although less promising at first, leads to results: patients register a cognitive improvement even if, unfortunately, there are not as many advances in language and movement. In short, in the future we will need both drugs that target amyloid in the early stages and molecules that act against Tau, in the more overt stages. Many tools for a complex disease, just like diabetes or oncology.
Alzheimer’s, another tile on the (first and only) therapy
by Simone Valesini
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