A new experimental Alzheimer’s drug is drawing attention for going after a different target.

Researchers reported Tuesday that Biogen’s diranersen may help slow early Alzheimer’s disease by lowering levels of tau, a brain protein tied to the illness. The findings were presented at the Alzheimer’s Association International Conference in London.

Tau is one part of a toxic duo fueling Alzheimer’s, but earlier efforts to develop drugs that target it have failed. Two approved Alzheimer’s drugs, lecanemab and donanemab, target the better-known amyloid protein and can modestly slow cognitive decline.

The new study, involving about 400 people, suggested diranersen did more than lower tau levels. Researchers found signs it also slowed cognitive decline, and in one small subset the effect was enough to be comparable to amyloid therapy.

Biogen plans a larger study to try to prove the drug’s benefit.

“This is really quite promising if it were to hold up” in that next-step testing, said Jessica Langbaum of the Banner Alzheimer’s Institute in Phoenix, who wasn’t involved with Biogen’s study.

“This is early days,” cautioned Dr. Reisa Sperling of Mass General Brigham, who also wasn’t involved in the study. But “I think it will reinvigorate interest and investment in lots of tau mechanisms, and the field needs that.”

It is not clear exactly what causes Alzheimer’s, which affects more than 7 million Americans and tens of millions of people worldwide. Amyloid starts building up in the brain about two decades before symptoms appear, forming plaques. Many scientists believe that buildup eventually triggers an abnormal form of tau to form tangles in neurons, setting off symptoms.

Diranersen is an antisense oligonucleotide. It does not attack tau buildup directly. Instead, it tells a tau-producing gene to make less of the protein.

“If you lower tau production, you are lowering the amount of the abnormal tau that needs to be cleared by the microglia, by the clearance mechanism in the brain. And so you are enabling the normal clearance mechanism to have more capacity to clear the tau,” said Dr. Cath Mummery of University College London, who led the study.

Today’s anti-amyloid drugs are delivered through the bloodstream by infusion or injection. Diranersen is injected into the fluid around the spinal cord.

Biogen’s trial enrolled people with mild cognitive impairment or mild Alzheimer’s and randomly assigned them to different doses of diranersen or a placebo. In May, Biogen and partner Ionis Pharmaceuticals said the lowest dose, given every six months, had the strongest effect. That result was unexpected and meant the study did not meet its planned goal of showing higher doses worked better.

Mummery said five of six brain tests showed that people who received diranersen still worsened in memory and other cognitive abilities, but more slowly than those who got dummy shots. In one test of the lowest dose, that meant a 26 percent reduction in cognitive decline, “approximately the same” change seen in earlier tests of amyloid drugs, she said.

Side effects included injection site pain and a temporary state of confusion that could appear a few days after the shot and last about a week, Mummery said. She said there were no signs of brain inflammation, which can affect recipients of anti-amyloid drugs.

The diranersen results come as researchers test other new approaches against Alzheimer’s.

The University of California, San Francisco, last week opened a first-of-its-kind study called the Alzheimer’s Tau Platform. Funded by the National Institutes of Health, it will test several experimental anti-tau therapies against, and in combination with, current amyloid treatments.

The first candidate is a vaccine called AADvac1, designed to train the immune system to recognize and fight a specific part of the tau protein, said UCSF’s Dr. Adam Boxer. He said the platform will expand to sites around the country, add other tau drugs and include people with Alzheimer’s-related protein buildup who do not yet have symptoms.

Researchers at the Alzheimer’s meeting also said an experimental cholesterol-lowering drug called obicetrapib might do more than help heart health. They are exploring if it also might lower buildup of Alzheimer’s-related proteins in people who carry the APOE4 gene, which is linked to genetic risk for the disease and also affects how the body processes cholesterol.

Obicetrapib maker NewAmsterdam Pharma plans to begin a study soon to test if the drug’s cholesterol effects also can mitigate Alzheimer’s risk in people carrying one or two copies of that gene.

Companies are also working on ways to get Alzheimer’s drugs into the brain faster and in higher volumes by getting through the brain’s protective lining. Denali Therapeutics CEO Ryan Watts described that approach as “hitching a ride” with iron that naturally gets into the brain.

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