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New cause of neuron death in Alzheimer’s

Alzheimer’s disease, expected to impact around 6.7 million people in the U.S. in 2023, causes a significant loss of brain cells, but the reasons for neuron death are not well understood.

A recent study from Northwestern Medicine suggests that RNA interference might be a key player in Alzheimer’s. Scientists have identified short toxic RNA strands linked to brain cell death and DNA damage in Alzheimer’s and aged brains. The study reveals a decrease in protective RNA strands during aging, potentially contributing to the development of Alzheimer’s.

The research also found that older individuals with superior memory, known as SuperAgers, have higher amounts of protective RNA strands. SuperAgers, aged 80 and older, show memory capacities similar to those 20 to 30 years younger.

Marcus Peter, the Tom D. Spies Professor of Cancer Metabolism at Northwestern University Feinberg School of Medicine, stated, “Nobody has ever connected the activities of RNAs to Alzheimer’s.” The study suggests a shift towards toxic RNA in aging brain cells.

The findings may have implications beyond Alzheimer’s, providing a new explanation for why neurodegenerative diseases start gradually as cells lose protection with age.

Moreover, this discovery opens a new avenue for treating Alzheimer’s and other neurodegenerative diseases. While existing drugs could be effective, further testing and improvements are needed.

The next step in the research is to determine the exact contribution of toxic RNAs to cell death in Alzheimer’s and screen for compounds that can selectively increase protective RNAs or block the action of toxic ones.

In plain terms, our gene information is stored in the form of DNA, but to turn this information into life’s building blocks, DNA needs to be converted into RNA. Short RNAs (sRNAs) have critical functions in cells, with one class suppressing long coding RNAs through a process called RNA interference. Some very short sequences in these sRNAs can cause cell death and are identified as toxic sRNAs, normally inhibited by protective sRNAs. MicroRNAs, a type of sRNA, act as guards preventing toxic sRNAs from damaging cells. However, the number of these guards decreases with aging, allowing toxic sRNAs to harm cells.

Key findings of the study include a reduction in protective sRNAs in the aging brain. Adding back protective microRNAs partially protects brain cells from cell death induced by Alzheimer’s triggers. Enhancing the activity of proteins that increase the amount of protective microRNAs inhibits cell death and completely blocks DNA damage seen in Alzheimer’s patients.

The study analyzed brains from Alzheimer’s mouse models, young and old mice, neurons from normal individuals and Alzheimer’s patients, and brains from SuperAgers. The research provides new insights into the understanding and potential treatment of Alzheimer’s disease.




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