There may be another explanation for the neuron death that contributes to the deficits of Alzheimer's disease. Short, toxic strands of riboneucleic acids or RNAs may allow Alzheimer’s to develop by killing brain cells, a recent study suggests.

In fact, interference in the translation of ribonucleic acid (RNA) into proteins may play a role in the development of Alzheimer’s and other neurodegenerative diseases. The findings, by researchers from Northwestern University, may eventually lead to new drugs to treat these diseases.

Cells contain long strands of RNA that code for proteins and short strands of RNA that do not code for anything. One class of short RNAs suppresses protein production by long RNA in a process called RNA interference. The researchers identified short strands of toxic RNA that block the production of the proteins necessary for the survival of brain cells, or neurons.

The strands of microRNA act as guards to prevent toxic RNA from entering the nucleus of the cell and blocking protein production. But the amount of protective microRNA decreases with age.

RNA interference by toxic RNA contributes to neuron death in older persons and those with Alzheimer’s disease.

These toxic RNAs are suppressed by short strands of protective RNA, called microRNA, in young, healthy people. The strands of microRNA act as guards to prevent toxic RNA from entering the nucleus of the cell and blocking protein production. But the amount of protective microRNA decreases with age.

The researchers also found that adding back protective microRNAs can partially protect neurons from cell death caused by the beta amyloid fragments that trigger Alzheimer’s disease. Enhancing the activity of the protein that increases the amount of protective microRNA partially inhibits the death of neurons from beta amyloid and prevents DNA damage also seen in Alzheimer's disease.

The researchers studied the brains of mouse models of Alzheimer’s disease, the brains of young and old mice, stem-cell derived neurons from both younger and older people and Alzheimer’s patients and human brain-derived neuron-like cells treated with beta-amyloid fragments that trigger Alzheimer’s. They also studied the brains of so-called SuperAgers, people over 80 years old who have the memory capacity of people 20 to 30 years younger.

“Our data support the idea that stabilizing or increasing the amount of protective microRNA in the brain could be an entirely new approach to stop or delay Alzheimer’s or neurodegeneration in general,” Marcus Peter, corresponding author on the study, told TheDoctor.

Further studies are needed to determine the exact way in which toxic short RNA contributes to cell death in neurodegenerative diseases and how best to screen for compounds that selectively increase the amount of protective microRNA and reduce the numbers of toxic short RNA.

The study is published in Nature Communications.