However, experts have also warned of sever side effects also noting that improvements were comparatively small.
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.
The adverse effects noted of the drug when administered included brain bleeds and swelling. The results showed 17.3 percent of patients administered the drug experienced brain bleeds, compared with nine percent of those receiving a placebo.
Alzheimer's Research UK said the findings were "momentous".
Eisai and Biogen had said in September that lecanemab - an antibody designed to remove sticky deposits of a protein called amyloid beta - reduced the rate of cognitive decline on a clinical dementia scale (CDR-SB) by 27% compared to a placebo.
Alzheimer's is a complex disease with multiple underlying causes tied to the biology of aging, therefore, the Alzheimer’s Drug Discovery Foundation (ADDF) has long held that a combination drug approach is needed, the study said.
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.
"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 per cent," 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 aging that can be combined to address the full array of underlying pathologies that contribute to the disease, said the study.
"Unique drug combinations matched to each patient's underlying pathologies is the answer, and our best hope 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.
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.
