The characteristic changes in the brain that occur with AD involve a build-up of two proteins: beta-amyloid (BA) and Tau. The increase in BA results in an overabundance of neuritic plaques in the brain that interfere with normal nerve transmission. The other protein, tau, leads to disordered tangles of nerve material, known as neurofibrillary tangles. Interestingly, most older people have both of these proteins in their brains, yet show no symptoms of AD. The reason why others do show symptoms of AD is because the BA and tau increases to abnormal levels in certain parts of the brain.
The statistics associated with AD are sobering. Currently, 5.3 million people are estimated to be afflicted with AD, and it is the 6th leading cause of death. It tends to strike those over 65 more frequently (13% of those over 65 have AD), although early-onset AD can show up as early as age 40. Every 68 seconds, someone becomes afflicted with AD. By 2050, that figure will rise to every 30 seconds, with 11-16 million people being diagnosed with AD. One in three seniors has AD. Women get it more often than men. Since 2000, the number of deaths from AD has risen by 68%, while deaths from other causes, including cancer and cardiovascular disease, have dropped.
As to the precise causes, there are many theories, and there may be more than one cause. For example, head trauma is known to increase both forms of abnormal AD proteins in the brain. Some suspect that today's athletes who are involved in sports that feature frequent head trauma, such as boxing and football, will later in life suffer from AD. Indeed, some of the greatest past champions, such as boxing legend, Sugar Ray Robinson, did get severe forms of AD late in life. Having two copies of a gene called APO-E4, increases the chances of acquiring AD by 80%. Having the genes doesn't guarantee the future development of AD, but does increase the risk. Recent research shows why APOE-4 is linked to AD. It lowers a protein called SIRT-1 that protects neurons. This implies that ingesting substances that may boost SIRT-1, such as resveratrol from red wine and quercetin, may offer some protection to those predisposed to AD because of having two genes for APOE-4. Fish oil offers some AD protection, especially the omega-3 fatty acid, DHA. However, the fish oil protective effect is negated in those with two APOE-4 genes. Green tea has also been shown in some studies to offer some AD protection if ingested chronically. Curcumin, which is contained in turmeric, has been shown in test-tube studies to not only prevent the build-up of BA in the brain, as well as Tau, but also to remove existing excess deposits of BA in isolated brain tissue. The problem with current curcumin supplements, however, is that they are rapidly converted in the liver to inactive metabolites, so that little or none enters the brain.
The most alarming aspect of AD is that there is no current effective way to prevent or treat the disease. However, the supplements mentioned earlier, through offsetting the buildup of abnormal BA and Tau, may offer some protection against the development of AD. The trick is that you have to start ingesting these supplements before the symptoms begin. Exercise is also effective at helping to prevent AD. It does this through boosting the level of brain-derived neurotrophic factor, which works by maintaining and repairing damaged brain cells. The increase in oxygen delivery to the brain offered by exercise also helps maintain neurons.
A new study that used mice as subjects found that a common food ingredient, also available in supplement form called phytosterols may offer potent protection against the onset of AD. Not all phytosterols were equally effective in this regard. The one that stood out was stigmasterol,which also happens to be the type of phytosterol least found in food sources. Those food sources include vegetable oils and nuts. Phytosterols are best described as "plant cholesterol,"since plants do not synthesize cholesterol. But phytosterols do have a close physical resemblance to cholesterol to the point where they can displace cholesterol in the intestines, thus reducing cholesterol uptake from food sources. As such, they are capable of lowering blood cholesterol levels by 7 to 10.5% on average, and when used concurrently with statin drugs, boost the cholesterol-lowering effect of statins significantly. At one point, phytosterols were sold as "anabolic" supplements, with the idea that, since cholesterol is the raw material used in the body to synthesize testosterone, phytosterols would do the same. Unfortunately, it doesn't work that way. However, some phytosterols, such as beta-sitosterol, seem to interfere with the activity of DHT, a byproduct of testosterone metabolism linked to prostate enlargement. In fact, beta-sitosterol is the active ingredient in the herb, Saw palmetto, often used to treat BPE.
In the new mouse study, stigmasterol was found to profoundly interfere with the synthesis of both BA and tau. In fact, it lowered the level of BA in mouse brain by a whopping 68%. It's important to note that while cholesterol is not the major player in cardiovascular disease as it has been long portrayed to be, in the brain, excess cholesterol is a definite stimulant to overproduction of BA. However, too little cholesterol in the brain is also associated with some forms of dementia. Ingesting stigmasterol may prove to be a way to control excess BA without interfering with normal cholesterol metabolism in the brain. Since this was a mouse study, it remains to be confirmed whether the same protective effect that occurred in the mice will also happen in human brains. But if it does, it will be far more effective as a preventive against AD onset than any existing drugs used to treat AD, all of which do little or nothing to halt the progression of the disease.
Burg, VK, et al. Plant sterols the better cholesterol in Alzheimer's disease? A mechanistical study.J Neuroscience 2013: in press.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
