Download PDF Copy Feb 12 2020
Researchers from Human Microbiology Institute (HMI) and Mitchell Center for Alzheimer’s disease at the University of Texas McGovern Medical School in Houston have discovered that bacterial extracellular DNA can trigger Tau protein misfolding into neurotoxic aggregates, a key process in Alzheimer’s disease pathogenesis. The discovery sets bacterial DNA as a new potential therapeutic target for treatment of neurogenerative illnesses. The breakthrough study is published in Nature’s Scientific Reports.
This is the first report showing that DNA from some bacterial species can promote Tau misfolding and aggregation - a hallmark feature of Alzheimer’s. In previous studies, George Tetz and colleagues demonstrated that the brain contains bacteria, as well as bacterial cell-free DNA, which get to the cerebrospinal fluid from systemic circulation due to an impaired blood brain barrier. In the current article, they show that bacterial DNA is capable to promote misfolding and aggregation of the Tau protein into aggregates that are similar to those found in the brains of patients with Alzheimer’s. Thus, bacterial DNA may act as a seeding and a promotional factor for Tau protein misfolding.
Recent data suggest that various bacteria are present in cerebrospinal fluid and postmortem brains of people with Alzheimer’s, but the role of brain-localized microorganisms has been elusive, until now.
This is the first report showing bacterial DNA playing a role in protein misfolding and aggregation, which may become a new target for the treatment not only of Alzheimer’s, but other neurogenerative diseases involving tau aggregation. The findings could have huge implications in how we fight a whole host of disorders. For decades, scientists have been frustrated with clinical trials failures in the Alzheimer’s space. So, this is a whole new hypothesis - we may have found a principally new lead not only for treating Alzheimer’s, but also for its prevention.” George Tetz, Head of Research and Development at HMI Related Stories
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