Replacing Neurons in Alzheimer's Patients?

Researchers from Northwestern University’s medical school say they have found a way to turn human embryonic stem cells into a type of nerve cell whose early death during Alzheimer’s disease causes memory loss.

The ability to grow these cells, known as basal forebrain cholinergic neurons, could help scientists figure out how to keep neurons from dying and eventually pave the way for healthy replacement neurons to be implanted in the brains of people with Alzheimer’s.

“This by itself is not going to cure the disease,” said Dr. Jack Kessler, chairman of neurology at the Northwestern University Feinberg School of Medicine and co-author of the stem cell study. “But eventually it can have a big impact on one of the biggest symptoms ... the one that bothers people the most, memory loss.”

Huntington Potter, an Alz­heimer’s researcher who has long been skeptical of stem cells as a potential treatment for the disease, called the Northwestern study a “real breakthrough.”

“The only problem is that [replacing lost neurons] doesn’t attack the disease itself,” said Potter, director of the Florida Alzheimer’s Disease Research Center, who was not involved in the research.

But using replacement neurons in combination with other therapies may be a promising approach, he said.

The findings were published Friday in the journal Stem Cells.

Embryonic stem cells, which are derived from embryos created for in vitro fertilization, are unspecialized cells that can be turned into cells with a specialized function.

Lead study author Christopher Bissonnette spent six years growing and testing millions of cells before figuring out how to activate the exact gene sequence needed to turn stem cells into cholinergic neurons.

His research team also found a way to create the neurons using skin cells from people with and without Alzheimer’s disease.

Bissonnette said childhood memories of watching his grandfather struggle with, and eventually succumb to, Alzheimer’s motivated him to search for new ways to treat the disease.

“I watched the disease slowly and relentlessly destroy his memory and individuality, and I was powerless to help him,” Bissonnette said. “That drove me to become a scientist.”

Source: Chicago Times