Common kitchen herb boosts memory and combats Alzheimer’s disease

Alzheimer’s disease is one of the most devastating illnesses of our time, affecting millions of people worldwide and ranking as the sixth leading cause of death in the United States. It robs individuals of memory, independence, and identity, while placing a heavy emotional and financial burden on families.

Despite decades of research, there is still no cure, and current treatments only slow symptoms modestly. But scientists are now looking toward nature for answers, and one familiar kitchen herb may hold surprising potential.

Alzheimer’s gradually destroys brain regions critical for memory and reasoning, particularly the hippocampus and cortex. The disease is marked by the buildup of sticky amyloid-beta plaques outside neurons and tangled clumps of phosphorylated tau proteins inside them. Together, these toxic proteins trigger inflammation and oxidative stress, damaging synapses—the vital connections between brain cells. Over time, the loss of these synapses closely mirrors the decline in cognitive abilities.

Researchers have long searched for treatments that can protect neurons from this destructive cycle. Many therapies have focused on removing amyloid plaques or tau tangles, but results have been mixed. Recently approved monoclonal antibodies that target amyloid can modestly slow decline, but they come with serious risks, including swelling and bleeding in the brain. Clearly, additional strategies are needed.

For centuries, rosemary and sage have been associated with memory. Shakespeare’s Ophelia even remarks, “There’s rosemary, that’s for remembrance.” Modern science is now revealing why. Both herbs contain carnosic acid, a plant compound with powerful antioxidant and anti-inflammatory effects.

Carnosic acid has a unique property: it stays inactive in healthy tissue but switches on when it encounters oxidative stress or inflammation. Once activated, it stimulates the Nrf2 pathway, a master regulator of the body’s defense systems against cellular damage. It also boosts heat shock proteins, which help cells refold misfolded proteins. These combined effects make carnosic acid an appealing candidate for combating neurodegeneration.

But there’s a problem. In its purified form, carnosic acid is unstable. It oxidizes quickly, making it unsuitable for use as a drug. Researchers needed a way to stabilize it without losing its therapeutic potential.

At Scripps Research, scientists led by Dr. Stuart Lipton tackled this problem by creating chemical derivatives of carnosic acid. One version stood out: a di-acetylated form known as diAcCA. This modified compound is stable on the shelf, converts efficiently into carnosic acid in the stomach, and is easily absorbed into the bloodstream. In fact, it delivers more carnosic acid to the brain than taking the original compound itself.

In a recent paper published in Antioxidants, the team reported that diAcCA not only showed excellent drug-like properties but also proved safe in toxicity tests. Since carnosic acid is already on the FDA’s Generally Recognized as Safe (GRAS) list, advancing diAcCA to human clinical trials may be faster than for most experimental drugs.

To test diAcCA, researchers used 5xFAD mice, a widely studied model of Alzheimer’s disease. These mice rapidly develop amyloid plaques, tau pathology, inflammation, and memory problems similar to those seen in humans. Over three months, the animals received daily doses of diAcCA.

The results were striking. In behavioral tests such as the Morris water maze and conditioned fear experiments, treated mice performed much better than untreated controls. Their learning and memory improved, suggesting that diAcCA restored some cognitive function.

When the scientists examined the animals’ brains, they saw why. Synaptic connections were preserved, amyloid plaques and phosphorylated tau aggregates were reduced, and inflammatory markers decreased. Importantly, diAcCA targeted inflamed brain tissue while remaining inactive elsewhere, minimizing the risk of side effects.

“By combating inflammation and oxidative stress with this diAcCA compound, we actually increased the number of synapses in the brain,” says Dr. Lipton. “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.”

One of the most promising aspects of diAcCA is its potential to work alongside existing treatments. Because it reduces baseline inflammation, it could make monoclonal antibody therapies safer by lessening their risk of brain swelling and bleeding.

“It could make existing amyloid antibody treatments work better by taking away or limiting their side effects,” Lipton explains. That possibility is especially important as new antibody-based drugs gain FDA approval and enter wider use.

In addition, the research team reported no toxicity in the digestive tract or other organs. In fact, diAcCA lowered background inflammation in the gut, hinting at broader protective effects.

While the spotlight is on Alzheimer’s, diAcCA’s benefits could extend to other disorders where inflammation and oxidative stress play a role. These include Parkinson’s disease, type 2 diabetes, and even heart disease. The compound’s unique “switch-on” mechanism in damaged tissues gives it versatility without the drawbacks of constant activation.

The findings also underscore the importance of looking to natural compounds as starting points for modern therapies. By tweaking molecules found in herbs, researchers may uncover treatments that are both effective and safer than many synthetic drugs.

Previous research has shown that the Nrf2 pathway, the one activated by carnosic acid, is often suppressed in Alzheimer’s patients. Animal studies using pure carnosic acid demonstrated improvements in learning and memory, as well as reductions in inflammation and toxic protein buildup. However, because the compound oxidized quickly and had poor bioavailability, its potential as a treatment was limited.

In earlier experiments, scientists tried delivering carnosic acid directly into the nose to bypass the digestive tract. These studies showed positive effects, but the method was impractical for long-term treatment in humans. The development of diAcCA was a direct response to these challenges, providing a stable, orally available alternative that retains all of the beneficial properties.

If these preclinical results translate into humans, diAcCA could offer a new class of therapy for Alzheimer’s disease. It would not only target amyloid and tau proteins but also address the underlying inflammation and oxidative stress that worsen the condition. This multipronged approach may slow disease progression more effectively than single-target drugs.

For families, that could mean more years of independence and preserved memory for loved ones. For healthcare systems, it could ease the enormous costs associated with dementia care. And because diAcCA is derived from a compound already considered safe, the path to clinical testing may be quicker than usual, potentially bringing hope sooner rather than later.

The research also sets a precedent for developing pro-drug versions of other natural compounds that are unstable but promising. By solving stability and delivery problems, scientists may be able to unlock a range of therapies hiding in everyday plants.

Note: The article above provided above by The Brighter Side of News.

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