Boswellic acids (K‐Vie™) improves clinical cognitive scores and reduces systemic inflammation in patients with mild to moderate Alzheimer’s disease.

Abstract

AbstractBackgroundAlzheimer’s disease (AD) remains an incurable neurodegenerative disorder. Neuroinflammation has been now recognized as an important player in the pathogenesis of AD. We conducted a clinical trial to measure whether boswellic acids (K‐Vie™, an enriched Boswellia extract) can improve cognitive and neuropsychiatric symptoms while reducing inflammation in patients with AD.MethodWe conducted a placebo‐controlled clinical trial including a total of 85 patients with mild‐to‐moderate (based on MMSE) Alzheimer’s disease randomized to Boswellia (n = 43) and placebo (n = 42) groups. The treatment doses were 400 mg K‐Vie™ capsule, thrice a day (1200 mg/day), versus matching placebo.ResultOf 85 patients, 43 were assigned to Boswellia and 42 to the placebo group. There were 8 dropouts. The median age of study participants was ∼71 (range, 63‐85) for the Boswellia and ∼70 (range, 61‐81) for the placebo group with 54.5% females and 45.5% males. After 6 months of treatment, there was a significant increase of the MMSE scores with a 1.7 (df = 39, 95% CI 1.2 to 2.1) unit in the Boswellia group compared to ‐1.4 (df = 36, 95% CI ‐2.0 to ‐0.9) unit decrease in the placebo group. There was also a significant decrease of the CDR‐SOB scores in the boswellia group with ‐0.8 (df = 39, 95% CI ‐1.1 to ‐0.6) unit difference, whereas the placebo group saw a 0.8 (df = 36, 95% CI 0.4 to 1.2) unit increase from baseline to 6 months. The analysis of neuropsychiatric symptoms (NPI‐Q) revealed a significant ‐3.4 (df = 27, 95% CI ‐6.1 to ‐0.8) unit decrease, whereas the placebo group did not show a significant change (p = 0.08) (df = 23, 95% CI ‐0.4 to 6.9). Patients receiving Boswellia showed a significant decrease as compared to placebo in plasma levels of several key pro‐inflammatory cytokines including IL‐6 (F(1,38) = 71.1, p<0.0001), TNF‐α (F(1,35) = 14.8, p = 0.0005), and IL‐1α (F(1,38) = 33.4, p<0.0001) as well as a significant increase in the plasma level of amyloid‐β42/amyloid‐β40 ratio (F(1,36) = 19.3, p<0.0001). No serious adverse events were observed during the trial.ConclusionThis study suggests that a reduction of systemic inflammatory biomarkers correlates with improvement in brain and cognitive function. Decreasing inflammation may represent a novel avenue to effectively treat AD.