Common kitchen spice linked to potential Alzheimer's biomarker reduction in new study

Taiwanese researchers report that sodium benzoate, a metabolite produced when cinnamon is metabolized, may help curb some Alzheimer's disease biomarkers and improve cognition in people with mild Alzheimer's disease. In a 24-week, randomized trial, participants given 750 mg or 1,000 mg daily showed significant reductions in amyloid-beta levels and improved scores on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) compared with a placebo. The study, published in Translational Psychiatry, also found that higher baseline levels of amyloid-beta 1–42 in the blood were associated with greater cognitive gains among those receiving the higher doses, a relationship not seen in the placebo group. Researchers note that the cinnamon-derived compound was safe and well tolerated, with a side-effect profile similar to placebo. They caution that the doses used are far higher than those found naturally in cinnamon and that dietary cinnamon cannot be expected to yield similar benefits.

Details of the trial: 149 participants aged 50 to 100 diagnosed with mild, early-stage Alzheimer's disease and elevated blood amyloid-beta were recruited from a Han Chinese population in Taiwan. They were randomly assigned to a placebo group or to daily capsules delivering 500 mg, 750 mg, or 1,000 mg of sodium benzoate. Cognitive function was assessed at baseline and after 24 weeks using the ADAS-Cog, a standard measure in Alzheimer's trials, while blood samples tracked amyloid-beta 1–40, total amyloid-beta, and other biomarkers. The design allowed investigators to compare all three active doses against placebo to gauge dose-response effects and safety.

At the 750 mg and 1,000 mg doses, cognitive performance improved significantly relative to placebo, and blood tests showed reduced levels of amyloid-beta peptides. The effect was strongest among participants who started with higher levels of amyloid-beta 42, indicating a possible interaction between baseline biomarker status and treatment response. The researchers reported that the treatment’s impact extended to two key amyloid measures, suggesting the compound may slow pathology linked to memory circuits in the brain. The authors emphasized that the results do not imply that cinnamon taken as a spice or in standard dietary amounts would confer protection, given that the active doses used are pharmacological.

Limitations include a moderate sample size and a 24-week duration, which leaves questions about long-term effects and safety unanswered. The researchers noted that the study was conducted in a Han Taiwanese population, and generalizability to other groups remains uncertain. While some earlier work has linked cinnamon-derived compounds to cognitive benefits in animal studies, the mechanism by which sodium benzoate would affect Alzheimer's pathology in humans remains unconfirmed. The broader field has seen other approaches targeting amyloid-beta proteins, including intravenous therapies that can slow cognitive decline but carry risks of brain swelling and bleeding, as well as high costs and demanding infusion schedules. The new findings align with a longstanding hypothesis that reducing amyloid-beta could support cognitive function, but they stop short of offering a ready-to-use dietary remedy.

Alzheimer’s disease affects roughly 7 million Americans, and rising birth rates and aging populations are expected to push cases higher in coming decades. Projections suggest that by 2060 about 13.8 million older Americans could have the disease if no cure emerges. The study’s authors say sodium benzoate has potential as a safer, more convenient option for amyloid-beta reduction, but they caution that more research is needed to confirm long-term benefits, optimal dosing, and the exact mechanism of action. Ongoing work in this area includes prior findings by researchers such as Dr. Kalipada Pahan, who in 2016 reported cinnamon may act as a slow-release form of sodium benzoate to improve learning and memory in animal models, and a 2023 synthesis of available studies suggesting that sodium benzoate can reduce amyloid-beta and tau in humans. The Translational Psychiatry paper notes that further trials are required to determine whether the observed biomarker changes translate into meaningful, sustained clinical improvement.