Scientists Protect Nerve Cells from Toxic Effect of Alzheimer’s Protein

Research published this week has identified a gene called Hes1, which appears to protect nerve cells from the toxic effects of the hallmark Alzheimer’s protein, amyloid. The study is published in the journal Alzheimer’s Research and Therapy.

One of the characteristic features of Alzheimer’s disease is the build-up of a protein called amyloid into plaques in the brain. These plaques can cause nerve cells to die, but the exact way this happens still remains to be understood.

The scientists, from the Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) in Spain, had previously discovered that amyloid can block the action of a protein called nerve growth factor, important for keeping nerve cells healthy. Their work showed that amyloid blocked a chain of events normally triggered by nerve growth factor, causing a reduction in the activity of a gene called Hes1. This appeared to prevent nerve cells from communicating effectively with each other, causing them to die.

In this study, the scientists took this research a step further, using their findings to develop new ways to protect nerve cells from amyloid. To do this, the team used mouse nerve cells, taken from an area of the brain called the hippocampus, known to be important for memory.

The researchers boosted Hes1 activity, either directly or by altering proteins known to control it, and found it could protect these nerve cells from the toxic effects of amyloid. The cells appeared healthier, had more connections and were more likely to survive when treated with amyloid. The laboratory findings suggest potential new strategies for blocking the effects of amyloid in human nerve cells.

Shirley Cramer CBE, Chief Executive of Alzheimer’s Research UK, the UK’s leading dementia research charity, said:
“Understanding what causes the loss of brain cells in Alzheimer’s is a key goal for the development of new treatments for this devastating disease. This study highlights an important molecular chain of events blocked by the hallmark Alzheimer’s protein amyloid. The results show that restoring the activity of this cascade could protect nerve cells in the lab against the toxic effects of amyloid.

“While there may be a long way to go before these findings could be turned into a potential new treatments in people, this kind of early stage research is vital for helping us piece together the puzzle. There are more than half a million people in the UK living with Alzheimer’s disease and that number is expected to rise. There must be a concerted effort to make research into dementia a national priority and secure long-term investment for research.”

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