Common herb restores memory and reduces inflammation for Alzheimer’s patients

Alzheimer’s disease is the most common cause of dementia and the sixth leading cause of death in the United States. It progressively damages brain regions responsible for memory and cognition, particularly the hippocampus and cortex.

As the disease advances, neurons deteriorate due to the buildup of toxic proteins, including amyloid-beta plaques and phosphorylated tau tangles. These aggregates contribute to oxidative stress, triggering neuroinflammation and further neuronal loss. Scientists have long searched for ways to slow or even reverse these effects.

The search for effective Alzheimer’s treatments has led researchers to explore compounds found in nature. Rosemary and sage contain carnosic acid, a plant-derived molecule known for its strong antioxidant and anti-inflammatory properties. “There’s rosemary, that’s for remembrance,” Ophelia declares in Shakespeare’s Hamlet. Now, modern science is investigating whether this age-old connection has merit.

Carnosic acid activates the Nrf2 pathway, a key regulator of the body’s defense against oxidative stress and inflammation. While promising, its instability makes it unsuitable for therapeutic use. The compound quickly oxidizes, limiting its shelf life and making oral administration ineffective.

To address this challenge, researchers at Scripps Research developed diAcCA, a chemically modified version of carnosic acid designed for greater stability and bioavailability.

A recent study published in Antioxidants demonstrates that diAcCA efficiently converts into carnosic acid in the stomach, allowing it to enter the bloodstream in therapeutic amounts. The researchers tested the compound in 5xFAD mice, a well-established model of Alzheimer’s disease, administering diAcCA for three months. The results were remarkable.

Mice treated with diAcCA showed significant improvements in learning and memory, as assessed through the Morris water maze and conditioned fear tests.

Examination of brain tissue revealed that diAcCA reduced amyloid plaques and phosphorylated tau aggregates, both hallmarks of Alzheimer’s pathology. It also restored synaptic density, a critical measure of neuronal connectivity that declines with disease progression.

“By combating inflammation and oxidative stress with this diAcCA compound, we actually increased the number of synapses in the brain,” says Dr. Stuart Lipton, senior author and professor at Scripps Research. “We also took down other misfolded or aggregated proteins such as phosphorylated tau and amyloid-beta, which are thought to trigger Alzheimer’s disease and serve as biomarkers of the disease process.”

Notably, diAcCA demonstrated a selective mechanism of action. It remained inactive in healthy tissues but became biologically active in inflamed regions, where it reduced neuroinflammation. This precision limits potential side effects while maximizing therapeutic benefits. Because diAcCA converts into carnosic acid, a compound already on the FDA’s Generally Recognized as Safe (GRAS) list, the path to human clinical trials could be accelerated.

Lipton’s research team found that diAcCA not only delivered more carnosic acid to the brain than taking carnosic acid alone, but it also displayed excellent pharmacokinetics. “DiAcCA produces more carnosic acid in the blood than if you took carnosic acid itself,” he explains. Importantly, the compound was well-tolerated by mice. Toxicity studies showed no adverse effects, and diAcCA even reduced baseline inflammation in the digestive tract.

The findings suggest that diAcCA could complement existing Alzheimer’s treatments. Current FDA-approved monoclonal antibodies target amyloid plaques but can cause side effects such as ARIA-E and ARIA-H—forms of brain swelling and bleeding. “It could make existing amyloid antibody treatments work better by taking away or limiting their side effects,” Lipton says.

Beyond Alzheimer’s disease, diAcCA’s anti-inflammatory and neuroprotective effects may extend to other conditions, including Parkinson’s disease, type 2 diabetes, and cardiovascular disease. The study’s success paves the way for human trials, bringing hope that a naturally derived compound could become a new weapon against neurodegenerative diseases.

As the global burden of Alzheimer’s disease continues to rise, the need for effective treatments has never been greater. While no cure exists, therapies that target inflammation and oxidative stress offer a promising avenue for slowing disease progression.

With diAcCA’s potential to improve cognition, protect neurons, and enhance existing treatments, it represents a crucial step forward in the fight against neurodegeneration.

Note: Materials provided above by The Brighter Side of News. Content may be edited for style and length.

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