'Zombie' Brain Cells Could Hold Key to Combating Alzheimer's, Mouse Study Suggests

Targeting so-called "zombie cells" could hold the key to treating age-related conditions, including Alzheimer's disease, according to a study on mice.

Also known as senescent cells, these units are neither useful nor dead, and are unable to replicate or develop distinctive characteristics. Scientists believe zombie cells group together in a way that could trigger the development of diseases such as Alzheimer's and Parkinson's, as well as physical ailments like osteoarthritis and atherosclerosis.

The researchers at the Mayo Clinic who did the study, which was published in the journal Nature, genetically modified mice to have tangles of the tau protein—believed to contribute to Alzheimer's disease—in their brains. They were also modified so senescent cells could be targeted.

The team found senescent cells collected in specific regions of the brain before mice experienced cognitive decline. Equally, stopping them from grouping seemed to stop tau proteins from clustering, and lessened neuronal death and memory loss.

Researchers targeted so-called zombie cells to understand their role in the development of age-related diseases. Getty Images

Darren Baker, a molecular biologist at the Mayo Clinic and senior author of the paper, told Newsweek: "Using a combination of unique mouse models and pharmacological means to eliminate these cells, we established that their presence in the central nervous system promotes pathologic alterations, including the accumulation of toxic aggregates of tau protein. Furthermore, we show that senescent cells drive neurodegeneration and loss of cognition in mice."

This research could have important implications for the treatment of age-related conditions, including Alzheimer's, which 5.7 million people in the U.S. are currently living with. By 2050, those numbers are expected to triple.

But we're still a long away from senescent cells forming the basis of treatments against such diseases.

"It is important to note that this study used mice we knew would be predisposed to disease," said Wilson. "We show that senescent cells have disease-promoting effects, now it will be important to establish if this occurs in other mouse models of neurodegeneration in patients."

James Pickett, the head of research at the Alzheimer's Society, who was not involved in the study, said: "There hasn't been a new dementia drug in 15 years, so it's exciting to see the results of this promising study in mice."

But he pointed out several barriers scientists must be overcome before a drug harnessing zombie cells hits the market.

"For example, we don't know if this drug is actually able to enter the brain, and older people often have lots of harmless brain cells that look like the senescent zombie cells this drug targets, so any treatment would have to be good at telling the two apart," he said.

Rosa Sancho, head of research at Alzheimer's Research UK, said: "Researchers are continuing to build a clearer picture of the precise interplay between the immune system and the brain, and this new work adds another piece to this puzzle."

She continued: "In this small but well-designed mouse study, researchers were able to clearly faulty immune cells from a region of the brain important for memory and thinking, and that doing so could limit damage associated with neurodegenerative diseases."