PNAs: protein β - arrestin-2 causes various forms of dementia

Protein β - arrestin-2 increases the accumulation of neurotoxic tau tangles by interfering with the removal of tau in the brain, which is the cause of various forms of dementia, according to a new study by the University of health of South Florida (USF) The researchers found that protein polymers composed of multiple β - arrestin-2 molecules are involved in the elimination of abnormal proteins, such as tau, which causes diseases Their findings are published today in PNAS The study focused on a disease called frontotemporal lobe degeneration (FTLD), which is one of the dementia after Alzheimer's disease This malignant dementia (45-65 years old) is characterized by atrophy of the anterior, lateral, or both regions of the brain Like Alzheimer's disease, FTLD also shows the accumulation of tau, and there is no effective treatment "Our research helps to develop new strategies to prevent FTLD," said junga (Alexa) woo, lead author of the paper and assistant professor of molecular pharmacology and physiology Previous studies have revealed that β - arrestin-2 has the ability to regulate the signal transduction of hormones and neurotransmitters in cells In addition, β - arrestin-2 can also form multiple interconnected units, which are called oligomers But the function of the latter is not clear In a recent paper published in PNAS, the authors found that in mice with increased tau protein content in the brain, the level of β - arrestin-2 increased at the same time In addition, when β - arrestin-2 was overexpressed, the tau content also increased Furthermore, by artificially reducing the level of β - arrestin-2, we can reduce the pathological deposition of tau protein and the symptoms of synaptic dysfunction and loss of connectivity between neurons and brain After that, we found that β - arrestin-2 oligomer reduced the efficiency of scavenging toxic tau in brain cells by blocking the activity of transporter p62 Blocking the oligomerization of β - arrestin-2 can inhibit the accumulation of pathogenic tau protein Beta-arrestin-2 increases neurotic tau driving frontotemporal dementia