UCSF Alzheimer’s Research Identifies Disease Could Be ‘Double-Prion Disorder’

May 2, 2019 | Alzheimer, Amyloid-beta, Tau

Nicholas Weiler reports for UCSF News that Alzheimer’s disease is a ‘double-prion disorder—self propagating amyloid and tau Prions found in post mortem brain samples with highest levels in patients who died young.  University of California, San Francisco researchers used novel laboratory tests the researchers detected and measured specific self-propagating prion forms of the proteins amyloid beta  (Aß) and tau in postmortem brain tissue of 75 Alzheimer’s patients. The UCSF research report high levels of prions in the brain samples were exceptionally associated with early-onset forms of Alzheimer’s disease and younger age at death.

The disease is defined upon observation of toxic protein aggregations in the brain known as amyloid plaques and tau tangles, accompanied by cognitive decline and dementia.  Attempts to treat the disease by cleaning out the inert proteins have failed. In a breakthrough for UCSF, new evidence that active Aß and  and tau proteins could be driving the disease could lead researchers to explore new therapies that focus on prions directly.  UCSF researchers published May 1, 2019 in Science Translational Medicine.

Lead Research/Investigator

Stanley B. Prusiner, MD, director of the UCSF Institute for Neurodegenerative Diseases and professor in the departments of Neurology and of Biochemistry and Biophysics.

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