In the wake of recent disappointments over clinical trials targeting amyloid plaque build-up in Alzheimer's disease, researchers are focusing more attention on misfolded tau protein, another culprit in brain diseases that cause dementia, Medical Xpress reports.

New research published in Science Translational Medicine finds that targeting abnormal tau through the suppression of a gene called MSUT2 (mammalian suppressor of tauopathy 2) shows promise.

Tau, like amyloid protein, is another substance that builds up in Alzheimer's disease and damages brain cells.

However, clinical trials targeting tau have been far less numerous in part because tau-targeted drugs have been hard to find.

In this study, researchers concluded that suppressing MSUT2 might protect people from Alzheimer's disease as long as the RNA binding protein PolyA Binding Protein Nuclear 1 (PABPN1) is not depleted. MSUT2 and PABPNI normally work together closely to regulate the biology of tau in the brain.

"If you inhibit MSUT2 and don't affect PABN1, that protects against the effects of tau pathology," said senior author Brian Kraemer, a research associate professor of medicine, Division of Gerontology and Geriatric Medicine at the University of Washington School of Medicine. He is also a scientist at the Veterans Affairs Puget Sound Health Care System.