Scientists work daily to find methods to disrupt pathways that create disease. For example, Alzheimer’s disease (AD) has several pathways – genetics, inflammation, oxidative stress, protein structural issues, excitotoxicity, and probably a few more less known.
I have written over forty articles on AD and continue to find new information, like today’s article, that provides another arrow in the quiver to address AD.
Latest Study
https://medicalxpress.com/news/2021-10-natural-compound-basil-alzheimer-disease.html. Fenchol is a terpene and can smell like pine, lemon, or camphor. It is found in basil and other plants. Medicinal properties associated with fenchol are antioxidant, anti-inflammatory, anti-microbial, anti-fungal, and analgesic (pain relief).
https://www.frontiersin.org/articles/10.3389/fnagi.2021.735933/full was published last week in the Frontiers in Aging Neuroscience. We have known for decades that there is a close link between the gut and brain. The gut microbiome is called the second brain.
Short-chain fatty acids (SCFAs) are produced in our gut. SCFAs create metabolites in our gut. Metabolites are the intermediary or end products of a metabolic process. Sometimes these processes produce energy, assist in growth or reproduction, or provide other maintenance functions for health. Metabolites drive various functions – signaling, stimulation, and inhibition.
The metabolites of SCFAs provide nutrition for our gut microbiome. As such, the health of the gut microbiome is linked to our brain health. Older adults with mild cognitive impairment have fewer SCFAs. A decline in SCFAs does not cause dementia or AD, but the linkage has scientists researching to find the cause-and-effect relationship.
Connection to Alzheimer’s
https://journals.physiology.org/doi/full/10.1152/physrev.00041.2018. SCFAs activate free fatty acid receptor 2 (FFAR2) receptors on neurons in the brain. When stimulated, brain cells (neurons) are protected against toxic accumulation of the amyloid-beta protein. Accumulations of amyloid-beta proteins are one of many pathways to AD. Neuron loss and death lead to neurological disease. Symptoms of neurological disease are loss of memory, erratic thinking, and other cognitive difficulties.
SCFAs metabolites stimulate FFAR2 that protect neurons from toxicity. When FFAR2 is inhibited in laboratory experiments, an abnormal buildup of amyloid-beta protein appears. There is a direct relationship between the level of FFAR2 and the appearance and accumulation of amyloid-beta proteins.
Nearly 150,000 natural compounds were screened to find those that could mimic the same natural biological effect of SCFAs metabolites in stimulating FFAR2. Our normal gut output of SCFAs is used up providing nutrition to many organs in our body before they reach the brain.
If researchers could find a way to target FFAR2 receptors on neurons specifically, then another tool is available to fight AD.
Fenchol binds to FFARs on neurons and stimulates the signaling processes. Laboratory animal studies showed that fenchol stimulated the FFAR2 receptor enough to reject neurotoxicity that supports the accumulation of amyloid-beta. In the presence of fenchol, amyloid-beta deposits were significantly reduced in the animal’s brain cells.
Upon close examination of the defense mechanism associated with fenchol binding to FFAR2, scientists discovered that fenchol decreased senescent neuronal cells (zombie cells) found in the brains of AD patients. Zombie cells accumulate in diseased and damaged tissues causing stress and death. They also send signals to surrounding healthy cells that can create similar conditions for growth and eventual harm to those healthy cells.
Fenchol stimulated FFAR2 to reject the neurotoxic pathway and addressed a side effect of zombie cells that exacerbate neurotoxicity in the brain. When amyloid-beta proteins were not allowed to aggregate on the neurons, they were swept away by the brain’s normal cleansing processes reducing the overall accumulation of amyloid-beta in the brain.
Conclusion
This is data derived from research and supports future studies to delve deeper into the cause-and-effect issues that support AD development. Adding extra basil to your Caprese salad or spaghetti might be premature. Human trials have not commenced. How humans process fenchol from basil is unknown. Is it bioactive and ready to stimulate FFAR2 receptors immediately? Or must it be isolated and refined a bit more?
Maybe a basil pill will be forthcoming? How fast does fenchol leave the gut and travels to the brain is also unknown. Will it hurt to add more basil to thwart the development of AD? I do not believe so.
Live Longer & Enjoy Life! – Red O’Laughlin – RedOLaughlin.com
