NIH works to better understand memory loss from neurodegenerative diseases
Tauopathies, a family of neurodegenerative disorders similar to Alzheimer’s disease, happen when the tau protein gathers inside brain cells. The new study shows that researchers can use an enzyme, caspase-2, to cut away tau. This may be important in reversing the disordered brain circuit function, which correlates with these illnesses.
To conduct the study, researchers used mice that were genetically engineered to copy factors of human tauopathy disorders. They were able to block caspase-2 activity to restore some memory as well as learning deficits. This suggests that it may be possible to heal the cognitive loss in tauopathies.
“The results of this exciting study suggest that the cognitive loss that occurs in tauopathy may be reversed by blocking the function of caspase-2,” Dr. Roderick Corriveau, program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), said. “This motivates further investigation of caspase-2 as a novel therapeutic target for dementia.”
NINDS funded the research, which was published in Nature Medicine.
“In the past, many studies focused on the accumulation of tangles and their connection to memory loss, but the more we learn, the less likely it seems that they are the cause of disease symptoms,” Dr. Karen Ashe, professor of neurology at the University of Minnesota and senior author of this study, said. “The pathological fragment of tau that we have identified resists forming tangles and can instead move freely throughout the cell. Therefore, we decided to look for other mechanisms that could affect synaptic function.”