Scientists have discovered a new therapeutic target for Alzheimer’s disease treatment. By reducing the accumulation of dangerous proteins in the brain, researchers may be able to prevent the disease or at least delay symptoms. The details are in a paper that was just published in the journal Neuron.
Alzheimer’s disease is a form of dementia that results in memory loss and impaired mental functioning. Currently, no cures exist but some symptoms can be managed with medication and therapy. An early sign of the disease is the accumulation of a toxic protein called tau. As tau builds up in the brain, it causes damage and increases the patient’s susceptibility to neurodegenerative illnesses.
Researchers from the Baylor College of Medicine, the Texas Children’s Hospital, and the Johns Hopkins University School of Medicine investigated possible ways to reduce levels of tau in the brain. They first looked for enzymes (proteins that can speed up chemical reactions) that might affect tau accumulation. After screening hundreds of possible enzymes in both fruit flies and cultured human cells, they found a candidate called Nuak1.
When the researchers inhibited Nuak1 activity, tau levels dropped in both human cells and Drosophila fruit flies. The fruit flies were a good model for monitoring enzyme activity since it allowed the scientists to see reactions in a complex, living system. Now that the team was sure of Nuak1’s role in tau build-up, they needed to confirm their findings with another animal model. When the researchers inhibited the enzyme in laboratory mice, tau levels dropped, brain damage was prevented, and the mice showed reduced dementia symptoms.
The team’s findings may allow researchers to develop a drug that reduces tau levels in the brain. This would prevent or at least delay Alzheimer’s disease. Since tau has also been linked to disorders such as progressive supranuclear palsy, a medication that reduces tau accumulation could help a lot of patients.
Lasagna-Reeves et al. Reduction of Nuak1 Decreases Tau and Reverses Phenotypes in a Tauopathy Mouse Model. Neuron (2016).