Alzheimer’s disease at the molecular level is in part characterized by the formation of Tau protein deposits in nerve cells. Metformin counteracts alterations of the cell structure protein Tau in mice nerve cells, according to a study from the German Center for Neurodegenerative Diseases (DZNE), the University of Dundee and the Max-Planck-Institute for Molecular Genetics.
“If we can confirm that metformin shows also an effect in humans, it is certainly a good candidate for an effective therapy on Alzheimer’s diseases,” said DZNE’s Sybille Kraub.
Tau is a molecule that usually binds to the supportive cytoskeleton and performs a function in the cell’s transport system, but in Alzheimer’s disease, Tau is tipped too strongly with phosphate groups, which causes removal of Tau from the cytoskeleton and aggregation.
Researchers attempted to regulate the protein PP2A, the protein normally responsible for removing phosphate groups from Tau protein. In Alzheimer’s, PP2A isn’t active enough, which leads to Tau deposition.
"So far there is no drug on the market that targets the formation of Tau aggregates," said Kraub.
The researchers added metformin to drinking water of healthy mice, which led to a reduction of Tau-phoshorylation in brain cells. Scientists also plan to investigate whether metformin prevents the deposition of Tau proteins in mouse models of Alzheimer’s disease and improve the animals’ congnition.
Since metformin is already used to treat diabetes, there is no risk of unexpected side effects when clinical trials in humans begin.