Skip to content

New Study Uncovers How Alzheimer’s Butchers Brain Cells

Alzheimer’s results in a substantial loss of brain cells known as neurons. 

How Alzheimer’s disease destroys a patient’s brain cells has been revealed in a new study. Alzheimer’s, which affects around 55 million people worldwide, results in a substantial loss of brain cells known as neurons.


Scientists have for a long while struggled to pinpoint the reasons behind this, but new research by Northwestern Medicine in Chicago has suggested that it may have something to do with RNA interference.


RNAs, also known as ribonucleic acids, are essential for most biological functions – but as a person ages, they can develop from being protective to being toxic.


Northwestern’s study found that short strands of toxic RNAs (sRNAs) can contribute to brain cell death and DNA damage, thereby playing a key role in the development of Alzheimer’s.

“Nobody has ever before connected the activities of sRNAs to Alzheimer’s,” said corresponding study author Dr. Marcus Peter.


“But we have found that, in aging brain cells, the balance between toxic and protective sRNAs shifts toward toxic ones.” The study’s findings have therefore pointed to potential new ways to treat Alzheimer’s.


As the disease is characterized by a progressive occurrence of amyloid-beta plaques, tau neurofibrillary tangles, and ultimately brain cell death, most scientists have focused on these avenues when trying to find a cure.


Dr. Peter explained: “The overwhelming investment in Alzheimer’s drug discovery has been focused on two mechanisms: reducing amyloid plaque load in the brain – which is the hallmark of Alzheimer’s diagnosis and 70 to 80 percent of the effort – and preventing tau phosphorylation or tangles.”

But these treatments have so far proved unsuccessful, meaning a different approach – like looking at sRNAs – may be the answer people have been looking for. “Treatments aimed at reducing amyloid plaques have not yet resulted in an effective treatment that is well tolerated,” said Dr. Peter.

“Our data supports the idea that stabilizing or increasing the amount of protective short RNAs in the brain could be an entirely new approach to halt or delay Alzheimer’s.”


He added that the research can also help with the treatment of other neurogenerative diseases, meaning the implications of the study are even wider. “We have a new explanation for why, in almost all neurodegenerative diseases, affected individuals have decades of symptom-free life and then the disease starts to set in gradually as cells lose their protection with age,” Dr. Peter said.


The study, published in Nature Communications, analyzed the brains of Alzheimer’s disease mouse models, the brains of young and old mice, neurons from individuals with and without Alzheimer’s, and a group of elderly people over 80 with memory capacity equivalent to those between 50 and 60 years old.


The researchers found that older patients, and those with Alzheimer’s, had more toxic sRNAs. Meanwhile, younger people, and those over 80 with the memory capacity of someone much younger, had more protective sRNAs.

RNAs should be used to produce proteins, but the team from Northwestern Medicine found that toxic RNAs can kill cells by blocking the production of proteins required for cells to survive.


Dr. Peter explained: “Our data suggests that these toxic sRNAs are involved in the death of neurons which contributes to the development of Alzheimer’s disease.

“The toxic sRNAs are normally inhibited by protective sRNAs. But their numbers decrease with ageing, thus allowing the toxic sRNAs to damage the cells.”


The next step in Dr. Peter’s research will be to determine in different animal and cellular models, as well as in brains of Alzheimer’s patients, the exact contribution of toxic sRNAs to the cell death seen in the disease.

He then intends to find compounds that would help increase the level of protective sRNAs or block the action of the toxic ones.


Produced in association with SWNS Talker

“What’s the latest with Florida Man?”

Get news, handpicked just for you, in your box.

Check out our free email newsletters

Recommended from our partners