As you know, I absolutely love science. I think that everyone should value what is currently happening in science because it affects medicine, technology, and how we view creation! For example, there was a recent study that changed the medical field when it comes to treating Alzheimer’s Disease. You can read my take on it below (Here’s the original article: https://advances.sciencemag.org/content/5/1/eaau3333).
It is common knowledge that brushing and flossing your teeth are important; together, they reduce cavities, prevent gingivitis, and keep your breath smelling fresh. A recent study published in the journal Science would add one more “plus” to that list – it could prevent Alzheimer’s disease. Although correlated with Alzheimer’s disease, chronic periodontitis (more commonly, gum disease) was never suspected to cause the neurodegenerative disease until now. New evidence published by Dominy and colleagues confirms the presence of the bacteria Porphyromonas gingivalis, a primary pathogen in gum disease, in the brain and the fluid surrounding the spinal cord (cerebrospinal fluid). More importantly, the study also suggests a role for the bacteria in destroying nervous tissue in the brain, which is a hallmark of Alzheimer’s Disease.
Alzheimer’s disease is most recognizable in our grandparent’s generation where this neurogenerative disease is the leading cause of dementia in people over the age of sixty.1 While most people recognize Alzheimer’s disease by behavioral changes (forgetfulness, uncontrollable emotions, inability to make decisions), scientists also note several key common features in the brains of affected patients. These include the formation of misfolded protein clumps both inside and outside cells, as well as an elevated inflammatory response. Both of these changes in the brain are associated with its response to bacterial or viral infection, though the precise pathogens involved in this response were previously unclear.1,2
The authors of this new study followed up on the previously recognized correlation between Alzheimer’s disease and gum disease, specifically focusing on the bacterium P. gingivalis. Having determined that this species of bacteria was a key predictor of Alzheimer’s disease in humans as well as in mouse models of infection, they sought to determine why P. gingivalis is so incredibly harmful to the human brain. One important feature that sets these bacteria apart from many other human pathogens is their preferred diet, which is composed of amino acids rather than sugars. Amino acids are the building blocks of proteins and can be obtained by degrading the structural proteins found in the oral cavity or other niches that P. gingivalis can inhabit. These bacteria actively cause the degradation of their host’s tissues by secreting a class of enzymes called gingipains, which chew up proteins and provide a steady supply of nutrients on which the bacteria can grow.
The authors hypothesized that bacterial secretion of gingipains in the brain was causing many of the pathological effects seen in Alzheimer’s patients. To test this hypothesis, they measured gingipain levels in both affected and non-affected brain tissue and also compared the enzymatic activities of these samples. They also tested the relationship of gingipains to other structural defects associated with Alzheimer’s disease, and were able to show a close correlation between these defects and the presence of gingipains. With this information, the researchers hypothesized that if they could inhibit the gingipain activity, they could slow or prevent the progression of Alzheimer’s disease.
By using mouse models of P. gingivalis infection, the authors demonstrated that common broad-spectrum antibiotics are ineffective at clearing the brain of bacteria, and perhaps explain why use of these drugs would not work as a treatment for Alzheimer’s disease. Instead they identified another class of drugs that can directly block gingipain action. This alternative approach not only blocked the activity of these enzymes, but also killed off the bacterial infection in the brains of mice and reversed the pathological effects similar to those seen in Alzheimer’s patients. Perhaps the most exciting aspect of this new class of drugs is that they can be taken orally and still get into the brain, which is relatively uncommon due to the isolation of the brain from other tissues. These drugs provide hope for a new avenue of treatment of a disease that is increasingly common and devastating to affected individuals. Who would have guessed that we could think about treating Alzheimer’s with similar methods to bronchitis – just a prescription antibiotic taken twice a day with water?
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