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Japanese pharmaceutical firm Eisai Co plans to seek full approval of its experimental Alzheimer's drug lecanemab in the United States, Europe and Japan armed with data showing it can slow the brain-wasting disease for people with early symptoms, potentially getting the treatment to patients next year. It remains unclear how widely the drug developed with U.S. biotech Biogen Inc will be used due to uncertainty over insurance coverage, including the U.S. government's Medicare plan for people age 65 and over, potential side effects and cost. One Wall Street analyst told Reuters news agency that he is not counting on measurable sales until 2024. Several estimated lecanemab may be priced at around $20,000 per year. "Most people who this (drug) would apply to are on Medicare, and most private payers look to Medicare as they make their own (coverage) decisions. So there's a massive roadblock in the way of all who could benefit from this treatment," said Robert Egge, Alzheimer's Association chief public policy officer. Eisai confirmed on Tuesday (November 30) that lecanemab - an antibody designed to remove sticky deposits of a protein called amyloid beta from the brain - reduced the rate of cognitive decline on a clinical dementia scale by 27% compared to a placebo. It also gave new details on side effects including a dangerous type of brain swelling and brain bleeding.

According to Alzheimer's Disease International, more than 55 million people worldwide will have Alzheimer's disease by 2020. This figure will nearly double every 20 years, reaching 78 million in 2030 and 139 million in 2050. The WHO Global Status Report for 2021 estimated the yearly global cost of dementia to be more than USD 1.3 trillion, with a projected increase to USD 2.8 trillion by 2030. To date most drugs developed to treat Alzheimer's disease have failed, largely because they target wrong biomarkers and individuals already exhibiting signs of the disease. Once symptoms appear, however, many brain cells responsible for memory and cognition are likely already damaged and beyond repair. Professor Shai Rahimipour in the Chemistry Department at Bar-Ilan University in Israel has pioneered a different approach utilizing theranostics to pinpoint and treat the earliest, pre-symptomatic signs of Alzheimer's disease. Showing promise in stopping progression of the disease before onset of irreversible brain cell damage, Rahimipour's groundbreaking approach has garnered significant attention in the scientific world.

Early detection and treatment of Alzheimer's disease require the use of dependable and cost-effective screening technologies. Researchers at Sweden's Karolinska Institutet have revealed that the level of tau, a protein that plays a vital role in the development of severe dementia, is associated with a kind of sugar molecule in the blood. The study, which is published in Alzheimer's & Dementia, can pave the way for a simple screening procedure able to predict onset ten years in advance. "The role of glycans, structures made up of sugar molecules, is a relatively unexplored field in dementia research," says the study's first author Robin Zhou, medical student and affiliated researcher at the Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet. "We demonstrate in our study that blood levels of glycans are altered early during the development of the disease. This could mean that we'll be able to predict the risk of Alzheimer's disease with only a blood test and a memory test." In Alzheimer's disease, the neurons of the brain die, which is thought to be a result of the abnormal accumulation of the proteins amyloid beta and tau. Clinical trials for Alzheimer's drugs show that treatment should commence early in the pathological process, before too many neurons have died, to reverse the process before it is too late.