But prevention may be in sight thanks to the work of researchers from Harvard Medical School, Dr. Rudolph Tanzi and Dr. Robert Moir, reports New Scientist.
Collections of plaque made from a sticky protein called beta amyloid has previously been correlated with Alzheimer’s, and led some scientists to think that the build-up may inhibit cell-to-cell signaling or trigger inflammation that causes immune system cells to attack surrounding cells. Dr. Tanzi, Dr. Moir, and their team have now shown that beta amyloid likely serves an immune function as an anti-microbial compound.
While, in theory, anti-microbial compounds should be beneficial, in practice they can seriously harm healthy cells. For example, as beta amyloid’s sticky plaque collects and kills bacteria, it also causes inflammation and blockages when the body doesn’t dispose of the trapped matter efficiently enough.
The researchers injected specialized mice brains with bacteria in order to test their theory and, sure enough, plaque promptly formed. According to Dr. Tanzi, the pathogenic threat didn’t have to be that significant – just a single bacterium could cause a plaque build-up overnight. This plaque interferes with surrounding neurons and causes them to malfunction or die.
The root cause in this case would be initial infections, which cause the beta amyloid bundles to form. The solution, therefore, may be to defend against infections in the first place, the researchers suggest. “You could vaccinate against those pathogens, and potentially prevent this problem arising later in life,” Dr. Moir told New Scientist.
More research is needed before any concrete conclusions can be drawn, but the experimental evidence suggests that vaccines might be a powerful weapon in the war against Alzheimers.
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