Compound found in rosemary shows promise for Alzheimer’s treatment

The herb Rosemary has long been linked to the memory: “There is Rosemary, that is for memory,” says Ophelia in Shakespeare’s Hamlet. It is therefore appropriate that researchers would study a connection in rosemary and sage-carnosic acid-for its impact on Alzheimer’s disease. In the disease, which is the main cause of dementia and the sixth most important cause of death in the US, inflammation is a component that often leads to cognitive decline.

Carnosic acid is an antioxidant and anti -inflammatory connection that works by activating enzymes that form the natural immune system of the body. Although pure carnosic acid is too unstable to be used as a medicine, scientists from Scripps Research have now synthesized a stable form, Diacca. This connection is fully converted into carnosic acid in the intestine before it is absorbed into the bloodstream.

The research, published in Antioxidants On February 28, 2025, when DiaCca was used to treat mouse models of Alzheimer’s disease, the therapeutic doses of carnosic acid reached in the brain and led to improved memory and synaptic density, or more synapses (representing the connections between nerve cells), in the brains. Because the deterioration of neuronal synapses is also closely correlated with dementia in Alzheimer’s disease, this approach can prevent the progression of cognitive decline.

Analysis of tissue samples showed that the drug also significantly reduced inflammation in the brain. This unique drug is activated by the inflammation that it subsequently fights and is therefore only active in parts of the brain that undergo inflammatory damage. This selectivity limits the potential side effects of carnosic acid, which is on the “grass) (grass) list of the US Food and Drug Administration, so that the road for clinical tests is relaxed.

By combating inflammation and oxidative stress with this diacca connection, we have even increased the number of synapses in the brain. We have also removed other incorrectly folded or aggregated proteins such as fosphorylored-Tau and amyloid-β, which is thought to activate Alzheimer’s disease and serve as biomarkers of the disease process. “

Stuart Lipton, MD, PhD, Senior Author, Professor, The Step Family Foundation Endowed Chair at Scripps Research and Clinical Neurologist in La Jolla, California

The group of Lipton had previously established that carnosic acid crossed the blood-brain barrier and activates the NRF2-transcriptional route, which engages antioxidant and anti-inflammatory genes. But the connection oxidizes easily, making it unsuitable as a medicine because of its short shelf life.

In this new study, Lipton and co-author Phil Baran, PhD, De Dr. Richard A. Lerner Endowed Chair in the Department of Chemistry at Scripts Research, synthesized a series of carnosaire acid drivers and selected Diacca as the best candidate because of stability, bio-availability and other drug-like properties. The Lipton group then treated mouse models with the connection over the course of three months. The group investigated the mice by testing their spatial learning and memory in behavioral tests and then analyzing brain tissue under the microscope.

“We have done several different memory tests and they were all improved with the medicine,” says Lipton. “And it not only delayed the decline; it almost improved normal again.” Analysis of tissues also showed increased neuronal synaptic density and reduced formation of phosphorylated Tau aggregates and amyloid-β-plaques.

The mice tolerated Diacca well. In toxicity studies, the connection calmed the baseline inflammation in the esophagus and even when it was converted into carnosic acid.

The group also discovered that the mice seized about 20% more carnosic acid after taking Diacca than after taking regular carnosic acid. Because most carnosic acid oxidizes while you are stored or with intake, “Diacca produces more carnosic acid in the blood than when you have taken carnosic acid itself,” explains Lipton.

Lipton sees a potential for Diacca to collaborate with Alzheimer’s treatments that are currently on the market. Not only could the medicine only work by combating inflammation, but “it could make existing amyloid antibody treatments better by removing or limiting their side effects”, such as a form of brain swelling or bleeding, known as Aria-E and Aria-H, he says.

Lipton hopes that Diacca can be followed quickly by clinical tests due to the safety profile. He thinks it can also be investigated as a treatment for other disorders characterized by inflammation, such as type 2 diabetes, heart conditions and other forms of neurodegeneration such as Parkinson’s disease.