Autophagy, or "self-eating," is an essential component of cellular survival and defense against invading organisms. It is how the cell degrades and recycles material into amino acids that can be reused. Several neurological disorders, including Parkinson's and Alzheimer's disease, are associated with the buildup of polypeptides within neurons.
Current evidence suggests that if the affected cells could break down these plaque buildups, it would greatly increase the chances of recovery. The ability to activate autophagy within these cells could prove invaluable in treating neurodegenerative disorders.
"Although we do not yet completely understand how these diseases develop, we do know that the proteins clump together and form a plaque buildup in affected patients' neurons," said Ann Progulske-Fox, Ph.D., a researcher on the study, in a press release. "If we can direct the cell's own ability to break down waste products against the plaques, we could keep them from forming and potentially intercept the development of these and other diseases."
In previous studies, Progulske-Fox and her colleagues demonstrated that the bacterium Porphyromonas gingivalis had the ability to activate autophagy when exposed to a human cell line, suggesting the bacterium secreted some unknown substance that initiated the process.
In the current study, the researchers report on a mutant strain of P. gingivalis (PG0717) that does not induce autophagy.
"Understanding how P. gingivalis turns on autophagy in host cells could lead to novel therapeutics for the treatment of neurodegenerative disorders, as well as advancements in the general understanding of the autophagic pathway," Progulske-Fox said. "Study of the mutant will facilitate this understanding and the development of new potential strategies for the treatment of multiple diseases."
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