If you read my previous post on Alzheimer’s (AD) you have some understanding that the way our bodies use and regulate lipids (fat and cholesterol) has impact on this pressing health issue.
Although amyloid beta – when pathological is one of the hallmarks of the plaque build-up associated with AD – is a protein, there is an unmistakable but not-yet-understood link between atherosclerotic plaque build up in the body and these plaque deposits in the brain.
It occurred to me that the mechanism our bodies use to digest fat is bile, which is produced by the liver and stored in the gall bladder. Because of the blood brain barrier it seems the bile produced in the body could not make it to the brain. But if it could, would bile somehow assist in plaque removal? It seems harebrained but I had to look. What I found was surprising.
In fact, bile is produced in the brain, independent of the liver, and levels in the brain under normal conditions are 10-fold higher than in the body’s circulation. In 2012 it was discovered that a bile acid present in both the liver and the brain, tauroursodeoxycholic acid aka TUDCA, directly reduced amyloid beta toxicity, acting as a potent neuronal cell protector. This research theorizes that TUDCA interferes with amyloid beta production and/or accumulation.
TUDCA-treated mice showed lowered inflammation, lowered amyloid beta deposits, and most importantly, rescued memory.
In 2018 a pharmaceutical company is set to test TUDCA in mild and moderate Alzheimer’s.
In 400 BC, as documented on silk fragments uncovered in a tomb in Hunan Province, dog and ox bile were recorded for the first time as treatments for various health disorders. In total, there are 44 different animal biles (including human) used as medicine in the ancient Chinese literature.
ApoE4 is a major genetic risk factor for late onset Alzheimer’s, it seems because the molecules die much more readily than ApoE3, so the plaque clearing mechanism is lost. TUDCA actually improves ApoE4 survival and function. One of the earliest effects of AD pathology is reduced synapse density, and synaptic loss is highly correlated with cognitive impairment. TUDCA modulates synaptic deficits induced by amyloid, rescuing synaptic loss. These are only two of the many effects TUDCA has on AD pathology in mice.
Given what we know, you do not have to wait for the expensive and protracted trials of the pharmaceutical powerhouses. Bile has been used, and documented as a treatment, for thousands of years.
As part of a diversified treatment plan for AD, I think we’re on to something.