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The first conditional go-ahead from the US drug regulator, the FDA, to a monoclonal antibody specifically targeted to slow the course of the disease has created great expectations. Alzheimer’s.
But we are only at the beginning of a journey, and not just because the FDA itself has requested new clinical trials. The drug, aducanumab, targets beta-amyloid, which is the compound that is deposited in the brain, creating a kind of “fog” that slowly isolates from the world and destroys memories and affects. The moncolonal antibody has been shown to be able to remove it, obviously in part. But we need to understand more, especially in perspective.
How does aducanumab work?
The monoclonal antibody can help modify the course of Alzheimer’s disease, counteracting cognitive and functional decline and helping sick people to remain independent for longer. But obviously it is not the definitive solution for the pathology which in Italy is responsible for about 60% of cases of cognitive impairment.
For this reason, even if we cannot speak of a definitive cure, the step forward achieved with the development path ofmonoclonal antibody bodes well. The research process began with the identification of protective anti-amyloid antibodies in healthy elderly people and in patients with dementia but with a very slowly progressing form of the disease, also demonstrating that these antibodies bound brain amyloid in the tissues of patients. Then, just by studying these antibodies that somehow naturally counteract the deposition of beta-amyloid, we came to identify aducanumab.
The drug is administered once a month, with a sort of “drip” that allows it to be introduced directly into the vein, and overcomes the blood-brain barrier, or that sort of “customs” that blocks the arrival of numerous compounds present in the blood to the nervous system. Once in the brain, the monoclonal antibody binds to brain amyloid and, together with the action of the immune system, helps to remove it.
Obviously, for this whole mechanism to be extremely useful, action must be taken soon. And this means arriving at the early diagnosis of the decay. The disease is characterized by the accumulation of beta-amyloid protein plaques, which begins approximately 15-20 years before the onset of symptoms. In this sense, the hope is that with the drug it is certainly possible not to eliminate the disease, but at least to slow down its evolution.
The other ways of research
While many wonder what the real-life effectiveness of this treatment, which will still be done on specific types of patients, can be, it must be said that we are not working only to develop intelligent “bullets” like this monoclonal antibody. The goal is to act on several factors: the first event to be countered is the accumulation with the consequent aggregation of beta-amyloid, which produces a dysfunction of brain activity.
But it is also necessary to work on the alteration of the Tau protein, fundamental for the vitality of neurons, which die in its absence. For this the therapeutic goal is to curb the accumulation of beta-amyloid, and possibly, the alteration of the Tau protein. In short, there are different paths in the world of research, even if today we know that we can hope to “tie” drugs to the pathological protein and drag it away, as does the garbage collection. We are only at the beginning, but it is important to understand that something is moving in the challenge of the disease that erases memories.
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