Is infection, or immune response, a contributing factor in neurodegeneration?. Credit: Prof. Jens Pahnke
There are many competing theories about the origin of Alzheimer’s disease but even if there is a singular origin, it’s not yet clear what that is. While the protein amyloid beta has been implicated in its pathology, and
recent development suggests a failure to clear the brain of this molecule may cause plaque formation, this protein may actually be part of an immune response in the brain, so removing it entirely could prove detrimental.
MRI of the head in a patient with benign familial macrocephaly. (Source: Wikimedia Commons)
Research at Harvard has
found that many of the genes associated with Alzheimer’s disease are centred upon the brain’s innate immune system. What’s more, the protein amyloid beta is very similar to a protein used as a defence against infection, LL-37, which also has a tendency to clump together. When amyloid beta was tested against microbes, it also killed many varieties, suggesting it may indeed have a defensive function. If this is in fact true, could it be that an infection, or inflammation and an exaggerated response to a foreign invader or molecule might trigger dementia? Parkinson’s disease has been connected to inflammation in the gut spread via the vagus nerve, so is it really so radical to suggest something similar may occur in a number of neurological conditions?
While this theory is still tenuous and may turn out to be a dead end, it raises interesting implications. Just as stomach ulcers can have a bacterial origin, something which took some time to work out, if these conditions do have a link to infection it could alter the approach to treatment. A company called
Cortexyme is currently working on a narrow spectrum antibiotic that could destroy an unspecified pathogen which may play a role, without harming the surrounding environment. When 43 Alzheimer’s brains were analysed in their studies, they all contained a bacterial protease enzyme and this particular bacterial strain seemed to increase amyloid beta levels, suggesting it could have a role.
“In healthy people some are clean but some do have small levels of this bacteria and its proteases. So we think that those people are on a path either to Alzheimer’s or maybe accelerated aging. We don’t know yet.”
The jury is still out on whether this approach has any merit, but considering the direct cause of Alzheimer’s disease is still unknown, imaginative approaches could prove beneficial.
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‘Are Microbes Stealing Your Mind?’
