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Article summary:

1. Researchers have found that an antibody treatment called lecanemab can reduce amyloid plaques, alter other biomarkers of Alzheimer's disease, and slow clinical decline in people with the condition.

2. The FDA has designated measurements of Aβ plaques taken by positron emission tomography (PET) as a ‘surrogate endpoint’ for clinical trials of this type.

3. Van Dyck and colleagues’ lecanemab trial provides a major boost to anti-Aβ treatments, and it is hoped that the phase III trial of donanemab will show similar benefits when findings are reported in mid-2023.

Article analysis:

The article is generally reliable and trustworthy, as it cites research from the New England Journal of Medicine and other sources to back up its claims. It also presents both sides of the argument fairly, noting potential risks associated with the drug trial for Alzheimer's disease as well as its potential benefits. However, there are some areas where the article could be improved upon. For example, it does not explore any counterarguments or present any evidence to refute them; it does not discuss any possible risks associated with taking lecanemab; and it does not provide enough detail about how the FDA determined that Aβ plaques were a suitable surrogate endpoint for clinical trials of this type. Additionally, while the article mentions that aducanumab was granted conditional marketing approval under the FDA's accelerated approval mechanism for serious conditions with an unmet medical need, it does not provide any information about what criteria were used to support this decision or how much financial coverage would be provided for treatments that modify Alzheimer's disease.