Alzheimer’s disease is usually associated with old age. But about 5% -10% of all cases of Alzheimer’s occur in people under 65. Alzheimer’s disease early progresses more rapidly and often affects people in the flower of life. The treatment options remain limited.
But the new data of a recent clinical trial suggest that an experimental medicine previously discontinued, called Gantenerumab, could help. The study found that Gantenerumab reduced the accumulation of amyloid plaques, one of the distinctive stamps of Alzheimer’s disease, in the brain. This can help delay cognitive deterioration in people with early start Alzheimer’s.
Alzheimer’s disease early is often related to genetic mutations in three specific genes. These mutations make the brain produce excessive amounts of beta amyloid, a protein that is grouped to form plates. These plates alter brain function, which causes memory loss.
Alzheimer’s disease early advances quickly, and the rapid decline is devastating. That is why researchers rush treatments that can delay the disease.
The recent clinical trial was a randomized stroke with placebo to evaluate the effects of Gantenerumab on people with early onset Alzheimer. The researchers monitored the changes in the cognitive skills of the participants and also used brain images and blood biomarkers (the presence of specific blood proteins that are related to Alzheimer’s) to trace the progress of the disease throughout the study.
The essay included 73 participants with rare hereditary genetic mutations that are known to cause early onset Alzheimer. These participants were asymptomatic or had mild symptoms of Alzheimer’s at the beginning of the study.
The results were intriguing. In a subgroup of 22 participants, who had not had any cognitive problems at the beginning of the study, taking the treatment for an average of eight years reduced the risk of developing symptoms of almost 100% probability to 50%. The brain scanners also showed a remarkable decrease in the accumulation of amyloid.
Gantenerumab is a monoclonal antibody, a protein designed in the laboratory to join the amyloid beta in the brain. When joining these plates, send a signal to the immune system to eliminate them. This could delay the progression of Alzheimer’s disease.
The drug acts by activating microglial cells. These are the main immunological defenders of the brain. Microglia constantly monitors the brain to detect damage and eliminate harmful substances, including amyloid beta. However, in people with Alzheimer’s disease, microglia often fails to remove the plaques efficiently. Gantenerumab improves this natural defense mechanism by marking amyloid plaques, which makes it easier for microglia to recognize and break down.
It is believed that beta amyloid plays a central role in Alzheimer’s disease by triggering inflammation, interfering with cellular communication and, ultimately, killing neurons. By eliminating these plates, the gantenerumab can help protect brain function. However, it does not revert the existing damage, so early intervention is fundamental.
An advantage of the Gantenerumab is that it can cross the blood brain barrier, the protective shield that blocks the arrival of many medications and harmful substances to the brain. This allows you to act directly on the amyloid plaques, which makes it more effective than some previous treatments that struggled with the administration of drugs.
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But despite what are these results, the Gantenerumab is not exempt from risks.
An important concern is the anomalies of amyloid -related images. It is swelling or small bleeding spots in the brain that appear in magnetic resonances. This is a common side effect of amyloid therapies.
In this last essay, 53 percent of the participants experienced these anomalies in amyloid -related images, including small cerebral hemorrhages in 27 percent of participants, brain swelling in 30 percent of participants and iron deposits per bleeding in 6 percent. While no participant had important cerebral hemorrhages or died due to treatment, these side effects remain a serious concern, since they require regular monitoring through brain scanners.
Another limitation is the modest cognitive benefit observed in the trial. While the Gantenerumab reduced amyloid plaques, it is not yet clear to what extent this translates into significant improvements in memory and thought skills.
The gantenerumab is also expensive to manufacture, which could make general access to if it obtains regulatory approval. Being an experimental drug, we currently do not know how much it will cost. But other similar anti-amyloid therapies, such as donanemab, currently cost around 25,000 pounds per patient per year.
The study also had a small sample size and only focused on a rare genetic form of early onset Alzheimer’s. More research is needed to see how these results can be applied to the dementia community in general.
Although the essay ended before the time after the study sponsor was withdrawn, these findings contribute to the ongoing debate on the causes of Alzheimer’s disease.
According to the amyloid hypothesis, the accumulation of amyloid plaques in the brain is the main cause of Alzheimer’s disease. The elimination of these plates will delay the progression of the disease. The success of the drugs for Alzheimer Lecanemab, Donanemab and now Gantenerumab, lend themselves to this theory.
This study also underlines the importance of early diagnosis. Therapies directed to amyloid seem to work better in the early stages of Alzheimer’s disease, before significant brain damage occurs. Advances in biomarker tests, including blood tests and brain scanners, could help to identify people at risk before. This would improve the efficacy of drugs such as Gantenerumab.
Although the Gantenerumab is not a cure and its manufacturer suspended it in 2022 because it did not demonstrate its effectiveness to slow down the progression of Alzheimer’s disease, these new data could lead to manufacturing Gantenerumab again. It also involves another step in the fight against Alzheimer’s.
Research on Alzheimer advances faster than ever. Either a success or a setback, each new study adds to our understanding of the disease and brings us closer to more effective treatments. For now, the essay with Gantenerumab offers a hopeful signal that scientists are progressing in the slowdown of the course of this devastating condition.
Information via The Conversation/Reuters.
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