“Alzheimer’s symptoms could be reversed by restoring protein in brain,” The Daily Telegraph reports.
Researchers say mice with Alzheimer’s disease-like symptoms showed improvement in memory tasks after being given the protein interleukin 33 (IL-33), which is thought to boost immune function.
They used mice bred to have Alzheimer’s-like symptoms to investigate whether injections of IL-33 into mice was able to reduce or reverse the symptoms of dementia.
People with Alzheimer’s have been found to have lower levels of IL-33. It is thought this could lead to the development of the abnormal clumps of proteins known as toxic beta-amyloid protein plaques, the characteristic hallmark of the condition.
Mice who received the protein had improved memory and brain function compared with the control group, as well as a reduction in beta-amyloid protein levels.
This is potentially very exciting as current treatments for Alzheimer’s can only temporarily slow the progression of the disease, as opposed to reversing the neurological damage it causes.
Of course, the normal warnings about prematurely assuming that positive animal results will translate into similarly positive results in humans apply.
Even if this treatment approach proves effective in humans, it remains to be seen if it would also be safe and free from significant side effects and complications.
Media estimates that it could take at least five years for this treatment to come to market – assuming it does prove safe and effective – seem reasonable.
Where did the story come from?
The study was carried out by researchers from a number of institutions, including the Hong Kong University of Science and Technology and the University of Glasgow.
Funding was provided by the Research Grants Council of Hong Kong SAR, the National Key Basic Research Program of China, a Hong Kong Research Grants Council Theme-based Research Scheme, and the SH Ho Foundation.
The study was published in the peer-reviewed journal, Proceedings of the National Academy of Sciences of the United States of America (PNAS) on an open access basis, so you can read it for free online.
This has been reported widely and accurately by the UK media, with a clear message that this is early research in mice and therefore caution should be taken – though many of the headline writers failed to pick up on this message.
Many of the reports include the somewhat world-weary, yet realistic, quote from lead author Professor Eddy Liew, who said: “Exciting as it is, there is some distance between laboratory findings and clinical applications.
“There have been enough false ‘breakthroughs’ in the medical field to caution us not to hold our breath until rigorous clinical trials have been done.”
What kind of research was this?
This is an experimental study in an animal model of Alzheimer’s disease that aimed to investigate whether injecting the interleukin 33 (IL-33) protein into mice leads to improved dementia symptoms.
IL-33 is a cell signalling protein, and previous studies have shown that levels of a receptor to “catch” IL-33 are increased in people with mild cognitive impairment (pre-dementia).
As the name suggests, cell signalling proteins play an important role in transmitting “messages”, or instructions, between cells.
This suggests that impaired IL-33 signalling could contribute to the development of the disease changes seen in Alzheimer’s, such as the build-up of beta-amyloid protein plaques.
The researchers therefore speculated there may be a role for IL-33 treatment to stop the changes of Alzheimer’s.
Animal studies like this are required to provide a path for further research in humans, but the findings are not directly applicable to people.
What did the research involve?
The researchers took mice aged between 6 and 25 months bred to have brains similar to people with Alzheimer’s. The mice were split into two groups: one group received IL-33 injections and the other was a control group.
IL-33 was given by injection into the abdomen for two consecutive days, after which time the two groups of mice were tested for symptoms of cognitive decline, including their:
- response to stimulus
- retrieval abilities, such as retrieval of fear memories following a fear conditioning test
These abilities were tested by putting the mice in an exploration chamber, which included features such as light beams and electric shock panels, for 15 minutes at a time on consecutive days.
After a further two days of IL-33 treatment, the mice’s brains were examined to look at the effect on amyloid plaques.
What were the basic results?
IL-33 was found to reach the brain within 30 minutes of injection and did not affect the general health of the mice.
The IL-33 group were found to have improved memory and cognitive function compared with the control group for learning, memory, response to stimulus and retrieval abilities. There was also a reduction in protein levels and the accumulation of amyloid plaques.
How did the researchers interpret the results?
The researchers concluded their findings indicate IL-33 is able to prevent and break down amyloid plaques, and even at late stages of the disease may represent a new treatment for Alzheimer’s disease.
This experimental study in mice aimed to investigate whether injecting the signalling protein interleukin 33 (IL-33) into mice leads to better outcomes in dementia.
People with Alzheimer’s disease have been found to have lower levels of the IL-33 protein in the brain than those who do not have the condition. The researchers hoped symptoms could be improved, or even reversed, by restoring levels of the protein.
These preliminary results are promising. In mice, IL-33 did seem to improve learning and memory in the exploration chamber tests, and also reduced beta-amyloid protein levels and the accumulation of amyloid plaques in their brains.
However, while these findings show promise, it is very early days – caution should be taken in interpreting these findings.
Studies in humans need to be conducted to see if such a treatment has the same effect and whether it is safe.
But human studies could take years, and even then we don’t know whether it would result in a licensed treatment.
As the exact cause of Alzheimer’s disease is still unknown, there’s no way to prevent the condition. But a good rule of thumb is “what is good for the heart is also good for the brain”.
Activities known to boost your cardiovascular health may also help reduce your dementia risk. These include:
- stopping smoking
- not drinking large amounts of alcohol
- eating a healthy, balanced diet, including at least five portions of fruit and vegetables every day
- exercising for at least 150 minutes (2 hours and 30 minutes) every week by doing moderate-intensity aerobic activity (such as cycling or fast walking) – this will improve both your physical and mental health
- make sure your blood pressure is checked and controlled through regular health tests
- if you have diabetes, make sure you keep to the diet and take your medication
Read more about preventing dementia.