Bacterial DNA promotes Tau aggregation
Human Microbiology Institute Research the First to Demonstrate that Bacterial DNA Trigger Alzheimer”s Disease
Research was presented at the Society for Neuroscience 2019. Society for Neuroscience was founded in 1969 by Ralph W. Gerard and, at nearly 37,000 members, has grown to be the largest neuroscience society in the world.
Chicago, IL October 19, 2019 — Human Microbiology Institute (HMI), a not-for-profit scientific research organization, today presented data that demonstrate for the first time how microbiome can trigger Alzheimer’s disease. The study, conducted by Drs. V. and G. Tetz, in collaboration with Claudio Soto was presented by Dr. G. Tetz in an oral session at Society for Neuroscience 2019 , October 19-23, Chicago, IL.
“This study for the first time suggests that bacterial DNA might be the initial seed that triggers the cascae of prion protein misfolding in Alzheimer’s disease” said George Tetz, MD, Ph.D., director, Human Microbiology Institute. “This study was designed to further investigate the potential us of bacterial DNA as a novel therapeutic target that may result in preventing this devastating disease”.
George Tetz states that a hallmark feature of Alzheimer’s disease and other tauopathies is the misfolding, aggregation and cerebral accumulation of tau deposits. Compelling evidence indicates that misfolded tau aggregates are neurotoxic, producing synaptic loss and neuronal damage. Misfolded tau aggregates are able to spread the pathology from cell-to-cell by a prion like seeding mechanism. The factors implicated in the initiation and progression of tau misfolding and aggregation are largely unclear. In this study, we evaluated the effect of DNA extracted from diverse prokaryotic and eukaryotic cells in tau misfolding and aggregation. Our results show that DNA from various, unrelated gram-positive and gram-negative bacteria results in a more pronounced tau misfolding compared to eukaryotic DNA. Interestingly, a higher effect in promoting tau aggregation was observed for DNA extracted from certain bacterial species previously detected in the brain, CSF or oral cavity of patients with AD. Our findings indicate that microbial DNA may play a previously overlooked role in the propagation of tau protein misfolding and AD pathogenesis, providing a new conceptual framework that positions the compromised blood-brain and intestinal barriers as important sources of microbial DNA in the CNS, opening novel opportunities for therapeutic interventions.