The protein amyloid beta is believed to be a major cause of Alzheimer’s disease. BACE inhibitors, which reduce the production of amyloid beta are therefore promising candidates for new drug treatments. A research team has recently demonstrated that one such BACE inhibitor reduces the amount of amyloid beta in the brain, restoring the normal function of nerve cells and improving memory performance. The team’s findings were published in the journal PNAS.

Using a mouse model of Alzheimer’s, the researchers tested a substance that inhibits beta secretase. In mice, as in humans, the disease causes amyloid beta plaques in the brain, which cause memory loss. In the study, mice were examined after having received the inhibitor in their food for up to eight weeks. Researchers observed individual nerve cells in the brain using an imaging technique called two-photon microscopy.

After the course of treatment, the mice had less amyloid beta in their brain, an unsurprising finding as its production was inhibited. However, their brain functions also normalised, with fewer hyperactive nerve cells and slow-wave brain patterns that were similar to those in healthy mice. Researchers also observed that the animals’ memory improved, with the treated mice finding a hidden platform in a water-filled maze as quickly as their healthy counterparts.

The scientists’ findings will soon find its way into clinical practice: a large-scale clinical trial is planned with around 1000 participants to test a slightly modified form of the BACE inhibitor.

Paper:“BACE inhibition-dependent repair of Alzheimer’s pathophysiology

Reprinted from materials provided by TUM.

November 28, 2017