An accumulation of beta-amyloid in the brain is one of the hallmarks of Alzheimer’s disease. Amyloid is a general term for protein fragments that the body produces normally. Beta-amyloid is a fragment snipped from an amyloid precursor protein (APP). In a healthy brain, these fragments are broken down and eliminated. In a brain with Alzheimer’s disease, the fragments accumulate and form hard plaques between neurons, blocking the transmission of messages and leading to the death of brain cells and, ultimately, dementia.
Celery contains a unique compound, 3-n-butylphthalide (3nB), that is responsible for both the vegetable’s characteristic odor and its health benefits. In animal studies, 3nB has been shown to:
- Lower blood pressure by acting as a diuretic and vasodilator
- Improve blood flow to the brain, protect against brain cell damage and enhance energy production within the brain
- Produce dramatic recovery in neurological and brain function studies that simulate a stroke
- Significantly increase lifespan in animal studies
- Exert anticancer effects and aid detoxification processes
- Improve cognitive performance and memory
Clinical research also indicates that celery seed extract appears to be particularly helpful for sufferers of gout, as 3nB appears to significantly lower the production of the uric acid that causes gout.
In a 2010 study of animals with Alzheimer’s disease, 3nB treatment significantly improved learning deficits as well as long-term spatial memory. 3nB treatment also significantly reduced total cerebral beta-amyloid plaque deposits and lowered brain beta-amyloid levels. In addition, researchers discovered that 3nB markedly directed amyloid precursor protein processing toward a pathway that precludes beta-amyloid formation. The researchers concluded that “3nB shows promising preclinical potential as a multitarget drug for the prevention and/or treatment of Alzheimer’s disease.”
Peng Y, Sun J, Hon S, Nylander AN, et al. L-3-n-butylphthalide improves cognitive impairment and reduces amyloid-beta in a transgenic model of Alzheimer’s disease. J Neurosci. 2010 Jun 16;30(24):8180-9.