
Alzheimer’s disease is the leading cause of dementia and affects millions of people around the world.
The disease slowly damages brain cells, causing memory loss, confusion, and difficulty with everyday activities.
As it progresses, people may lose the ability to recognize family members, communicate, or live independently. Although researchers have studied Alzheimer’s for decades, there is still no cure, making the search for better treatments one of the biggest challenges in medicine.
For many years, scientists have focused on a sticky protein called amyloid, which forms plaques in the brain many years before symptoms begin. This work led to newer medicines such as lecanemab and donanemab.
These drugs remove amyloid from the brain and have been shown to slow memory decline, but only by a modest amount. They also carry risks, including brain swelling and bleeding in some patients. Because of these limitations, researchers have continued looking for other ways to slow the disease.
One of the most promising targets is another brain protein called tau. Healthy tau helps support nerve cells, but in Alzheimer’s disease it becomes abnormal and forms tangles inside brain cells. Many experts believe amyloid starts the disease process, while abnormal tau is more closely linked to the loss of memory and thinking ability that follows.
Now researchers have reported encouraging early results for an experimental drug called diranersen. The findings were presented at the Alzheimer’s Association International Conference in London. The study suggests the medicine may slow early Alzheimer’s by reducing the production of tau rather than trying to remove tau after it has already built up.
The research involved about 400 people with mild cognitive impairment or mild Alzheimer’s disease. Participants were randomly assigned to receive different doses of diranersen or a placebo. Unlike current anti-amyloid medicines that are given through the bloodstream, diranersen is injected into the fluid around the spinal cord, allowing it to reach the brain more directly.
Diranersen belongs to a newer class of medicines called antisense oligonucleotides. Instead of attacking existing tau tangles, it works by telling the gene responsible for making tau to produce less of the protein. Researchers hope that lowering tau production gives the brain’s natural cleaning systems a better chance to remove abnormal tau before it accumulates.
Although the trial did not meet its original main goal because the lowest dose unexpectedly worked better than higher doses, the results still attracted considerable attention. Five of six cognitive tests suggested that people receiving the medicine experienced slower worsening of memory and thinking. In one important measure, the lowest dose reduced cognitive decline by about 26 percent, a benefit similar to that reported in earlier studies of some amyloid-targeting drugs.
The treatment also appeared to have a different safety profile. Some participants experienced pain at the injection site and temporary confusion lasting about a week after treatment, but researchers did not observe the brain inflammation sometimes seen with anti-amyloid medicines.
Scientists are also exploring many other tau-based treatments. Researchers at the University of California, San Francisco have launched the Alzheimer’s Tau Platform, a large research program that will test several experimental anti-tau therapies, including a vaccine designed to train the immune system to recognize harmful tau.
Other companies are investigating ways to transport medicines into the brain more efficiently and even whether cholesterol-lowering drugs might reduce Alzheimer’s risk in people with certain high-risk genes.
If you care about Alzheimer’s disease, please read studies about the protective power of dietary antioxidants against Alzheimer’s, and eating habits linked to higher Alzheimer’s risk.
For more health information, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
Source: Alzheimer’s Association International Conference.


