New Delhi: If there is one disease that has kept scientists and doctors flummoxed over the years, proving the fallibility of human ingenuity, it is Alzheimer’s — the debilitating disease that lays a patient’s mind to waste. Now, a new drug holds the promise of stemming the progress of the dreaded disease.
The U.S. Food and Drug Administration (FDA) is expected to give a full approval to Leqembi, the brand name for the drug Lecanemab, for the treatment of Alzheimer’s Disease later this week.
A monoclonal antibody medication, it is the second of a new category of medications approved for Alzheimer’s Disease in the US after Tacrine, which is used to treat mild to moderate Alzheimer’s Disease.
Leqembi, too, is for patients with mild cognitive impairment or in the mild dementia stage of disease — the population in which treatment was studied in clinical trials.
Monoclonal antibodies are a type of protein that are made in the laboratory and work against certain conditions such as cancer and different other diseases by binding to specific targets in the body.
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What is Alzheimer’s disease?
Alzheimer’s is an irreversible, progressive brain disorder that slowly destroys cognitive function, memory and thinking skills, and eventually the ability to carry out simple tasks.
It is caused by the formation of abnormal protein structures, called plaques, outside the brain’s neurons. These plaques are made up of a protein called beta-amyloid that disrupts the normal functioning of the brain. The beta-amyloid plaques can build up between the neurons, affecting the communication between them. As a result of these changes, the neurons in the brain become damaged and eventually die.
This leads to a loss of connections between the neurons, affecting memory, thinking, and other cognitive functions. Over time, as more and more neurons are affected, the symptoms of Alzheimer’s disease become more severe.
Protofibrils are intermediate structures that form during the aggregation process of beta-amyloid proteins in Alzheimer’s disease. It is an indicator of early-stage onset of Alzheimer’s and promotes degeneration of neural cells.
How does Leqembi work?
Leqembi consists of an antibody — that was first isolated from mice and then designed in its current form for humans — that binds with protofibrils. By doing this, the drug claims to prevent plaque build-up in the brain, and eventually slow down or halt the progression of Alzheimer’s Disease, potentially improving cognitive function in affected individuals.
Last year, researchers evaluated Leqembi’s efficacy in a clinical trial of 856 patients with Alzheimer’s disease, over a 79-week period.
Treatment was initiated in patients with mild cognitive impairment or mild dementia stage of disease and confirmed presence of beta amyloid plaques.
Patients receiving the treatment had significant reduction of beta amyloid plaques, the researchers claimed.
The patients received the approved dose of lecanemab, 10 milligrams per kilogram of body weight, every two weeks, showed significant reduction in brain amyloid plaque in 79 weeks, according to an FDA note.
On the basis of these results, Leqembi was taken up under the Accelerated Approval pathway, which the US FDA uses to approve drugs for serious conditions, where there is an unmet medical need.
What are the current risks associated with the drug?
The use of Leqembi is not without risks, however.
It includes a warning for amyloid-related imaging abnormalities (ARIA), which are known to occur with antibodies of this class.
ARIA may cause temporary swelling in areas of the brain that usually resolves over time and may be accompanied by small spots of bleeding in or on the surface of the brain. Some people may have symptoms such as headache, confusion, dizziness, vision changes, nausea and seizure.
Another warning for Leqembi is for a risk of infusion-related reactions, with symptoms such as flu-like symptoms, nausea, vomiting and changes in blood pressure.
(Edited by Poulomi Banerjee)
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