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Popular Alzheimer’s theory may be wrong
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Inflammation has long been thought to play an essential role Alzheimer’s disease (AD). However, scientists in the US and Germany are not so convinced. In a new paper published in Acta Neuropathologica, University of Florida [UF] scientists argue that there is no significant sign of chronic inflammation in AD brains, effectively challenging one of the most strongly held hypotheses in the field.
Microglia have long been implicated as the perpetrators of inflammation-related AD complications. Microglia are cells of the immune system; they are scavengers that ingest and destroy harmful molecules in the brain. They also cause inflammation. Short-term inflammation is good; it is a signal to other parts of the immune system that something is wrong. However, long-term—or chronic—inflammation can cause damage. It is thought that chronic stimulation by microglia actually causes increased production of amyloid plaques, a hallmark of AD pathogenesis.
Researchers at UF and University of Frankfurt, Germany looking at human brain tissue “discovered that inflammation of microglia…does not appear to be associated with dementia in Alzheimer's disease.” [UF] This evidence is contrary to a multitude of research conducted in mouse models, which have shown chronic inflammation to be a key problem in AD. In fact, there has even been conclusive research that shows treatment with anti-inflammatories attenuates the effects of AD, including the prevention of memory deficiencies.
But Wolfgang Streit, a professor of neuroscience at the College of Medicine, states, "In the current paper we have shown that the brain's immune system, made up of microglia, is not activated in the brains of Alzheimer's patients, as would be the case if there were inflammation.” [UF] One possibility for the discrepancy in results could be that previous studies were carried out in mice. It is not entirely unheard of for mouse models to not accurately portray the corresponding human system. If true, the new study would shake up the AD field. No inflammation means no immune system activation which means that mouse models for AD are not as reliable as previously thought. Such a theory is radical—and sure to stir up controversy.
Currently, a daily dose of an anti-inflammatory drug like ibuprofen is a recommended technique to stave off the pressures of dementia—though there has been no definite proof of their effectiveness. But if this new study is correct, then such measures do nothing to help protect against the formation of diseases such as AD.
Important people are certainly listening. Mark A. Smith, editor-in-chief of the Journal of Alzheimer’s Disease, says, "This paper potentially represents a paradigm shift in the way we look at Alzheimer's disease. The study goes against the very popular idea of neuro-inflammation; instead, the idea that microglia are senescent is consistent with a number of features of the disease.” [UF]
Senescence is the idea that cells (and in turn, organisms) decline in ability and effectiveness with age, and is the new theory Streit and his team are suggesting. Instead of chronic activation of microglia, the cells are silent and ineffective to the point that the immune system is unable to protect neurons when AD begins to set in. The images of human brain tissue taken by Streit shows degenerated and aged microglia, not large, activated microglia which would indicate inflammation. He believes that the evidence supports an entirely new direction in research, one that leads away from the two-decade-old hypothesis of inflammation.
"What I expected to see is activated microglia right next to dying neurons," Streit said. "That is what I did not find. What I propose is glia are dying, and the neurons lose support. We now need to find out what caused glia to degenerate. Rather than trying to find ways to inhibit microglia with anti-inflammatory drugs, we need to find ways to keep them alive and strong. It's a whole new field." [UF]
The study is, of course, preliminary. Only 19 brains were imaged. That’s 19 brains against 20 years of research. It will be interesting to watch this story develop. Serious challenges against popular theories are normally met with considerable opposition. There is no doubt that such a strong claim will be investigated by more scientists, but the truth of the matter may still be a long time in developing.
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