Researchers at the University College London have found through recombinant dog proteins that a protein called Keap1 may be the new target of preventing Alzheimer's disease (AD) and other neurodegenerative diseases. The role of Keap1 is to inhibit the Nrf2 protein with protective neuronal function. By inhibiting the function of Keap1, the researchers can activate the Nrf2 protein function, protecting the nerve cells in the pathological environment without damage.

The current treatment of AD is still at ease in the level of AD symptoms, and there are no drugs to prevent the production of AD or prevent further deterioration of the disease in the market. The Nrf2 transcription factor receives the attention of researchers because of the ability to protect brain cells from stress in stress conditions. And cell stress enhancement is an important feature of many neurodegenerative diseases. In AD patients, the function of Nrf2 was inhibited. Therefore, the researchers attempted to treat neurodegenerative diseases by increasing the expression of Nrf2 or activating the function of Nrf2.

A potent Nrf2 activator has been developed and has been shown to play a role in protecting nerve cells from neurotoxicity and improving memory deficits in AD mouse models. However, these activators also cause serious side effects due to off-target effects, and over-activation of Nrf2 can also cause other side effects. Therefore, to find a way to minimize the activation of Nrf2 method is a great issue for researchers to complete.

In this study published in PLOS Genetics, the researchers found that β-amyloid in the Drosophila model inhibited Nrf2 function. Keap1 is a natural Nrf2 inhibitory factor. When the researchers used genetics to reduce the expression of Keap1 in the Drosophila model, they found that this could enhance Nrf2 activity and reduce the cytotoxicity of amyloid. Further studies have found that lowering Keap1 levels can increase the degradation of amyloid in the Drosophila model. In the mouse cell culture model, the researchers found that a newly-developed inhibitor that binds Keap1 to Nrf2 can reduce the synergistic effect of amyloid on mouse neuronal synapses.

"The importance of our work is that it shows that blocking Keap1 compounds can improve the activity of Nrf2 in protected cells, so they are likely to prevent neuronal cell death in AD and other Alzheimer's patients," said Dr. Fiona Kerr, the lead author of the article. "Keap1 may be an effective target for preventing neuronal damage in AD. We need more work to develop this inhibitor that inhibits the interaction of Keap1 with Nrf2 into a drug that can be used in animal experiments and to detect whether this strategy can protect human nerve cells from AD damage." Flarebio provides superior recombinant proteins such as recombinant NPP1 at competitive prices.