Gum Disease May Trigger Alzheimer

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Hints of the bacterium Porphyromonas gingivalis, which causes chronic gum disease, have been found in the brains of individuals who had Alzheimer‘s disease. The outcome proposes the bacterium may assume a job in driving the improvement of the disease, research delivered in Science Advances.

Specialists saw brain tissue from post-mortems of people with and without Alzheimer’s disease and found a larger part of those with the infection had more elevated amounts of a compound called gingipains, which is sourced by P. gingivalis. They likewise examined the chemical’s belongings in the brains of mice, and found that it made the animals create indications of Alzheimer’s. The outcomes demonstrate gingipains is the “primary driver of Alzheimer’s disease,” consider coauthor Steve Dominy, a neurologist at Cortexyme, Inc., an organization creating medications for the diseases. The new research is one of a developing number that recommend microorganisms assume a job in Alzheimer’s disease.


Dominy, S. S., et al. (2019). “Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors.”  5(1): eaau3333.

Yale Researcher Devise drinkable cocktail for Alzheimer Therapy

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drinkable Alzheimer cocktail

Yale researchers have fabricated a drinkable cocktail of designer mix that meddles with a pivotal initial step of Alzheimer’s and even reestablishes memories in mice, reported in Cell Reports.


The binding of amyloid beta peptides to prion proteins triggers a course of destruction measures in the advancement of Alzheimer’s — collection of plaques, a damaging immune system reaction, and harm to neural synapses.


"We needed to discover particles that may therapeutically affect this immune system response," said senior author Stephen Strittmatter, the Vincent Coates Professor of Neurology, professor of neuroscience, and director of the Yale Alzheimer Disease Research Center.


Erik C. Gunther, et al., “Rescue of Transgenic Alzheimer’s Pathophysiology by Polymeric Cellular Prion Protein Antagonists,” Cell Reports, 2018; doi:10.1016/j.celrep.2018.12.021