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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.

A new study published in The Lancet has revealed that a total of 1.7 million people could be living with dementia in England and Wales by 2040. The research highlighted increasing numbers of people who will suffer from Alzheimer's. The disease would massively increase the burden on the healthcare system. The research was led by University of College London (UCL). Lead researcher, Dr Yuntao Chen said, "It is shocking to think that the number of people living with dementia by 2040 may be up to 70 per cent higher than if dementia incidence had continued to decline. "Not only will this have a devastating effect on the lives of those involved but it will also put a considerably larger burden on health and social care than current forecasts predict.

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.

The first big breakthrough in 30 years of Alzheimer's research is providing momentum for clinical trials of "cocktail" treatments targeting the two hallmark proteins associated with the mind-robbing disease, according to interviews with researchers and pharmaceutical executives. Drugmakers Eisai and Biogen reported in September that their therapy lecanemab could slow progress of the disease by 27% over 18 months compared with a placebo. The finding validates the theory that clearing the amyloid protein that forms clumps in the brains of Alzheimer's patients could slow or halt the disease and has strengthened the support from some scientists for simultaneously targeting another notorious protein linked to Alzheimer's: tau. Eisai and Biogen are scheduled to present full data from their lecanemab study on Tuesday at the Clinical Trials on Alzheimer's Disease conference in San Francisco. The U.S. Food and Drug Administration is expected to make a decision by early January on the companies' application for accelerated approval. If approved on an accelerated basis, the companies said they would immediately apply for full U.S. regulatory approval which could help secure Medicare coverage.

In a new study, men who took phosphodiesterase type 5 inhibitors (PDE5Is), such as Viagra (sildenafil; Pfizer), for treatment of erectile dysfunction, were found to be 18 per cent less likely to develop Alzheimer's compared to those who did not take the drugs. The results of the population-based cohort study were published in Neurology on 7 February 2024. Researchers at University of Oxford examined IQVIA Medical Research Data UK records of 269,725 men, who were diagnosed with erectile dysfunction between January 2000 and March 2017. None of the participants had any memory or thinking problems at the start of the study and they were followed for an average of 5.1 years. During the study, 749 out of 1,119 participants taking erectile dysfunction drugs developed Alzheimer's disease.

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.

Alzheimer's disease is an irreversible brain disorder that destroys memory and thinking skills. It progressively makes simple tasks difficult to achieve.

An experimental Alzheimer's drug developed by Eli Lilly and Co slowed cognitive decline by 35% in a late-stage trial, the company said on Wednesday, providing what experts say is the strongest evidence yet that removing sticky amyloid plaques from the brain benefits patients with the fatal disease. Lilly's drug, donanemab, met all goals of the trial, the company said. It slowed progression of Alzheimer's by 35% compared to a placebo in 1,182 people with early-stage disease whose brains had deposits of two key Alzheimer's proteins, beta amyloid as well as intermediate levels of tau, a protein linked with disease progression and brain cell death. The study also evaluated the drug in 552 patients with high levels of tau and found that when both groups were combined, donanemab slowed progression by 29% based on a commonly used scale of dementia progression known as the Clinical Dementia Rating Scale (CDR-SB). Using that scale, experts said Lilly's findings were roughly on par with Eisai Co Ltd and Biogen Inc's lecanemab, sold under the brand name Leqembi, which reduced cognitive decline by 27% in patients with early Alzheimer's in a study published last year. The results drove Lilly's shares to a record high, up more than 6% at $429.85. Dr. Ronald Petersen, an Alzheimer's researcher at Mayo Clinic, said Lilly's trial is the third to show removing amyloid from the brain slows progression of the disease, which could put to rest some lingering doubts about the benefits of drugs in the class and the amyloid-lowering theory. "It's modest, but I think it's real," he said of the benefit, "and I think it's clinically meaningful." Dr. Erik Musiek, a Washington University neurologist at Barnes-Jewish Hospital, said the efficacy looks as good or better than lecanemab.