New Alzheimer’s drug found effective in reducing cognitive decline: Study

Alzheimer's disease begins with a brain protein known as amyloid beta. The protein starts building up into plaques two decades or more before people show the first signs of neurological problems.

Los Angeles: A new drug, lecanemab, has been found to slow down cognitive decline in Alzheimer’s patients, according to a study that could lead to new treatments for the neurodegenerative disease.

The study results were presented at the 15th Clinical Trials on Alzheimer’s Disease (CTAD) Conference in San Francisco, US, on November 29. The study is also published in the New England Journal of Medicine.

Amyloid-clearing and cognitive decline-slowing drug lecanemab, which is poised for FDA approval early next year, will be a positive step in the treatment of Alzheimer’s, the study said.

Alzheimer’s is a complex disease with multiple underlying causes tied to the biology of ageing, therefore, the Alzheimer’s Drug Discovery Foundation (ADDF) has long held that a combination drug approach is needed, the study said.

Alzheimer’s Drug Discovery Foundation (ADDF) is dedicated to rapidly accelerating the discovery of drugs to prevent, treat and cure Alzheimer’s disease.

“Today’s results show that lecanemab slows cognitive decline, which is welcome news for the millions of patients and families living with Alzheimer’s,” said Dr Howard Fillit, Co-Founder and Chief Science Officer at the ADDF.

“But this is only a start to stopping Alzheimer’s in its tracks. We have a lot of ground to cover to get from the 27 per cent slowing lecanemab offers to our goal of slowing cognitive decline by 100%,” said Fillit.

Amyloid-clearing drugs are one part of the solution, but there remains a pressing need to develop a new generation of drugs targeting all aspects of the biology of ageing that can be combined to address the full array of underlying pathologies that contribute to the disease, said the study.

New and emerging easy-to-use diagnostic tools like those supported by the ADDF’s Diagnostics Accelerator can help pinpoint the specific underlying causes of each person’s Alzheimer’s, enabling precision treatment approaches and improving clinical trials, said the study.

“Unique drug combinations matched to each patient’s underlying pathologies is the answer, and our best hope is to give patients long-lasting relief from this insidious and progressive disease,” said Fillit.

Today’s Alzheimer’s drug pipeline is more robust than ever, with 75 per cent of drugs currently in clinical trials aimed at novel targets beyond amyloid and tau according to a recent report.

“Today’s news is encouraging for everyone who has worked on lecanemab and for those of us who have spent decades tackling Alzheimer’s by improving clinical trial designs,” said Fillit.

“But even more, this is proof that our research is paying off. It gives us a clear vision of a day soon when treatments will allow patients to maintain their independence not just for weeks or months more, but for years more and perhaps for their lifetimes,” said Fillit.

Alzheimer’s disease begins with a brain protein known as amyloid beta. The protein starts building up into plaques two decades or more before people show the first signs of neurological problems.

After years of amyloid accumulation, tangles of tau – another brain protein – begin to form. Soon after, tissues in the affected areas begin to wither and die, and cognitive decline sets in.

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