Alzheimer, a new drug could slow cognitive decline
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A new drug could slow cognitive decline due to Alzheimer’s disease. This is supported by a study by the University of California, San Francisco, published in Jama. With the expected approval of a third new Alzheimer’s drug by the Food and Drug Administration, the industry is starting to show progress in the fight against the disease.
“Medications work best for people in the early stages of Alzheimer’s, and other therapies will be needed to help people with advanced disease,” he said Gil Rabinovicidirector of the University of California, San Francisco’s Alzheimer’s Disease Research Center affiliated with the Memory and Aging Center, the departments of Neurology, Radiology, and Biomedical Imaging at the University of California, San Francisco, and the Weill Institute for Neurosciences.
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“This is likely just the beginning chapter of a new era of molecular therapies for Alzheimer’s disease and related neurodegenerative disorders,” Rabinovici said in an editorial in JAMA, published alongside results from the latest drug, donanemab. Rabinovici did not participate in the trial.
The monoclonal antibody
Donanemab is a monoclonal antibody, like the two previous Alzheimer’s drugs, aducanumab and lecanemab. These drugs attack brain plaques which are made up of a protein called amyloid. They disturb cell function and lead to the rapid spread of another protein called tau. Both amyloid and tau contribute to the development of Alzheimer’s disease. The study showed that donanemab slowed cognitive decline by 35% compared to placebo, in patients with low to medium tau levels in the brain. These results are similar to those obtained with Leqembi, which received FDA approval earlier this month.
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In the donanemab study, patients also had a 40% lower risk of progressing from mild to mild dementia or mild to moderate dementia. Donanemab proved to be the best drug in circulation for the removal of amyloid plaques, even compared to Aduhelm and Leqembi. The medicine reduced tau concentrations in the blood, but not in a key area of the brain. Patients in a more advanced stage of disease showed little or no benefit compared with those who received the placebo.
“Combined with the drug’s potentially serious side effects, this should prompt experts to aim higher in developing more effective and safer treatments,” Rabinovici wrote. Donanemab should be limited to patients with low to medium tau levels, indicating mild disease. Other studies are evaluating the efficacy of monoclonal antibodies in the early stage of the disease, before symptoms appear. Like two other new Alzheimer’s drugs, donanemab has been associated with ARIA, amyloid-related imaging abnormalities that can include brain swelling and microhemorrhages. Severe ARIA occurred in 3.7% of patients, including three deaths. The risks were higher among patients with the APOE4 gene, which is linked to a higher risk of Alzheimer’s.
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Genetic tests
“For this reason – said Rabinovici – genetic tests should be recommended before treatment with monoclonal antibodies”. Although ARIA has generally been safely administered in clinical trials, Rabinovici urged caution as these drugs enter real practice and suggested limiting access to patients with normal MRIs before treatment, repeating the resonances at regular intervals and to interrupt or suspend the treatment when the AIR occurs. Lack of ethnic diversity was a major limitation of the study. Only 8.6% of the 1,251 US participants were non-white.
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“The study raises ethical concerns about the generalizability of the findings to higher-risk populations, showing higher rates of dementia in black and Latino populations,” Rabinovici concluded. patients, it may make sense to limit the duration of treatment to the time needed to clear the amyloid plaques from the brain. This could greatly improve the feasibility of treatment for patients, doctors, insurers and health systems.”
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