Tau proteins are involved in more than twenty neurodegenerative diseases, including various forms of dementia. These proteins clump together in patients’ brains to form neuronal tangles: protein aggregation that eventually coincides with the death of brain cells. Researchers have now discovered how tau disrupts the functioning of nerve cells, even before it starts forming tangles.
The study was published in Nature Communications.
In healthy circumstances, tau proteins are connected to the cytoskeleton of nerve cells, where they support the cells’ structural stability. In the nerve cells of patients, however, tau is dislodged from the cytoskeleton and ultimately tangles together to form protein accumulations that disrupt the nerve cell’s functioning.
But even before these protein accumulations are formed, the dislodged tau impedes the communication between nerve cells. The researchers say that they found that across fruit flies, rats, and human patients, dislodged tau ends up at nerve cell synapses, where it hooks into vesicles and inhibits communication between different nerve cells.
The next step, the researchers say, is to see if, in animal models, they can find ways to keep tau from hooking onto vesicles and, by extension, prevent nerve cell death.
Paper: “Tau association with synaptic vesicles causes presynaptic dysfunction”
Reprinted from materials provided by: VIB – Flanders Interuniversity Institute for Biotechnology