Dr. Mary Newport, Coconut Oil, Ketones, and Dementia

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Protection against Alzheimer’s Disease

Growing evidence suggests that turmeric may afford protection against neurodegenerative diseases. Epidemiological studies show that in elderly Indian populations, among whose diet turmeric is a common spice, levels of neurological diseases such as Alzheimer’s are very low. Concurrently, experimental research conducted recently found that curcumin does appear to slow the progression of Alzheimer’s in mice. Preliminary studies in mice also suggest that curcumin may block the progression of multiple sclerosis. While it is still unclear how it may afford protection against this degenerative condition, one theory is that it may interrupt the production of IL-2, a protein that can play a key role in the destruction of myelin, the sheath that serves to protect most nerves in the body.

A number of studies have suggested that curcumin, the biologically active constituent in turmeric, protects against Alzheimer’s disease by turning on a gene that codes for the production of antioxidant proteins. A study published in the Italian Journal of Biochemistry (December 2003) discussed curcumin’s role in the induction of the the heme oxygenase pathway, a protective system that, when triggered in brain tissue, causes the production of the potent antioxidant bilirubin, which protects the brain against oxidative (free radical) injury. Such oxidation is thought to be a major factor in aging and to be responsible for neurodegenerative disorders including dementias like Alzheimer’s disease. Another study conducted jointly by an Italian and U.S. team and presented at the American Physiological Society’s 2004 annual conference in Washington, DC, confirmed that curcumin strongly induces expression of the gene, called hemeoxygenase-1 (HO-1) in astrocytes from the hippocampal region of the brain.

Curcumin Crosses Blood-Brain Barrier, May Help Prevent Alzheimer’s Disease

Research conducted at UCLA and published in the Journal of Biological Chemistry (December 2004), which has been confirmed by further research published in the Journal of Agricultural and Food Chemistry (April 2006), provides insight into the mechanisms behind curcumin’s protective effects against Alzheimer’s disease.

Alzheimer’s disease results when a protein fragment called amyloid¦Â accumulates in brain cells, producing oxidative stress and inflammation, and forming plaques between nerve cells (neurons) in the brain that disrupt brain function.

Amyloid is a general term for protein fragments that the body produces normally. Amyloid¦Â is a protein fragment snipped from another protein called amyloid precursor protein (APP). In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer’s disease, the fragments accumulate, forming hard, insoluble plaques between brain cells.

The UCLA researchers first conducted test tube studies in which curcumin was shown to inhibit amyloid¦Â aggregation and to dissolve amyloid fibrils more effectively than the anti-inflammatory drugs ibuprofen and naproxen. Then, using live mice, the researchers found that curcumin crosses the blood brain barrier and binds to small amyloid- species. Once bound to curcumin, the amyloid- protein fragments can no longer clump together to form plaques. Curcumin not only binds to amyloid-Â, but also has anti-inflammatory and antioxidant properties, supplying additional protection to brain cells.

Turmeric Boosts Amyloid Plaque Clearance in Human Alzheimer’s Patients

The most active ingredient in turmeric root, bisdemethoxycurcumin, boosts the activity of the immune system in Alzheimer’s patients, helping them to clear the amyloid beta plaques characteristic of the disease.

In healthy patients, immune cells called macrophages, which engulf and destroy abnormal cells and suspected pathogens, efficiently clear amyloid beta, but macrophage activity is suppressed in Alzheimer’s patients.

Using blood samples from Alzheimer’s patients, Drs. Milan Fiala and John Cashman have shown that bisdemethoxycurcumin boosts macrophage activity to normal levels, helping to clear amyloid beta. Fiala and Cashman also observed that bisdemethoxycurcumin was more effective in promoting the clearance of amyloid beta in some patients’ blood than others, hinting at a genetic element. Further study revealed the genes involved are MGAT III and Toll-like receptors, which are also responsible for a number of other key immune functions. Bisdemethoxycurcumin enhances the transcription of these genes, correcting the immune defects seen in Alzheimer’s patients. Proc Natl Acad Sci U S A. 2007 Jul 31;104(31):12849-54.