Alzheimer’s disease is a big problem, especially in places like the U.S. where about 6.7 million people were affected by it in 2023.
This disease causes a lot of brain cells to die. But understanding why these cells die has been a tough question for scientists.
Recently, a team of scientists at Northwestern Medicine made a breakthrough. They found out that something called RNA interference might be really important in Alzheimer’s.
For the first time, they discovered tiny bits of RNA that are harmful and can lead to brain cell death and DNA damage in people with Alzheimer’s and in older brains. They also noticed that small bits of protective RNA decrease as we get older, which might let Alzheimer’s develop.
Interestingly, the study showed that really old people with amazing memory (called SuperAgers) have more of these protective RNA bits in their brains. SuperAgers are people who are over 80 but have a memory as good as people who are 20 to 30 years younger.
Marcus Peter, who led the study, said this is the first time anyone has linked RNA activity to Alzheimer’s. He explained that in aging brains, there’s more harmful RNA than protective RNA.
Their research, published in Nature Communications, could be important not just for Alzheimer’s but for other brain diseases too.
Peter said that their findings might explain why people can live for many years without symptoms and then start showing signs of these diseases as they get older and lose their protective cells.
New Hope for Treatment
This discovery opens up new ways to treat Alzheimer’s and maybe other brain diseases. Alzheimer’s is known for certain features like amyloid-beta plaques, tau tangles, and finally, the death of brain cells.
A lot of the efforts to find a cure for Alzheimer’s have focused on reducing amyloid plaques, which are a key sign of the disease, or preventing tau tangles. But so far, treatments that try to reduce amyloid plaques haven’t been very successful.
Peter and his team think that increasing the amount of protective RNA or stabilizing it in the brain could be a new way to stop or slow down Alzheimer’s or other brain diseases.
There are already drugs that might do this, but they need more testing in animals and improvement.
The next step for Peter and his team is to figure out exactly how harmful RNAs contribute to cell death in Alzheimer’s.
They want to do this by studying different animal and cell models and brains from Alzheimer’s patients. They also want to look for better drugs that can increase protective RNAs or block harmful ones.
What are These RNAs?
To understand this better, let’s talk about RNA. Our genes are stored as DNA in every cell’s nucleus. DNA is turned into RNA, which helps make the proteins our bodies need. RNA is essential for many of our body functions.
There are two types of RNAs: long ones and short ones. The short RNAs (sRNAs) don’t make proteins but have other important jobs. One of these jobs is called RNA interference, where they can stop the long RNAs from making certain proteins.
Peter’s team found very short sequences in some sRNAs that can kill cells by stopping the production of essential proteins. This leads to cell death. They think these toxic sRNAs play a role in neuron death in Alzheimer’s.
Normally, protective sRNAs stop these harmful sRNAs. MicroRNAs are one kind of protective sRNA. They work like guards, keeping the harmful RNAs from doing damage. But as we age, we have fewer of these guards, letting the harmful RNAs cause damage to the cells.
The scientists looked at brains from different sources: Alzheimer’s disease mouse models, young and old mice, neurons from normal and Alzheimer’s patients, brains of SuperAgers, and human brain-derived neuron-like cell lines treated with amyloid beta, which is linked to Alzheimer’s.
This extensive study helped them understand the role of these RNAs in Alzheimer’s disease.
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For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and coconut oil could help improve cognitive function in Alzheimer’s.
The research findings can be found in Nature Communications.
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