Summary: More inflammation is tied to a higher risk of dementia and Alzheimer’s disease. But new studies show that high levels of some inflammatory markers may point to less mental decline in Alzheimer’s. The study enrolled adults with proven amyloid beta deposits (sticky protein clumps) in the brain but mostly normal thinking. These people had high levels of the cytokines (immune signals) IL-12 and IFN-γ.
Alzheimer’s disease is a leading cause of disability and death in the Western world. What is worrying is that after more than a century of research, science still knows too little about it. Think about it. There is no reliable test to diagnose Alzheimer’s early. Worse, no test can reliably predict how the disease will progress. Science does know that amyloid and tau proteins build up and brain cells die. But the role of these proteins in the disease is far from clear. For example, not everyone with amyloid in the brain gets Alzheimer’s. There is still much to learn.
Many studies suggest that low systemic inflammation may raise Alzheimer’s risk. But a new study shows that some inflammatory markers may be tied to a lower risk of mental decline in Alzheimer’s. So not every inflammatory response means higher Alzheimer’s risk. There is a reason for these mixed findings. Inflammation is very complex. Hundreds of proteins take part in it. Inflammation that runs unchecked for a long time may raise the risk of chronic disease. But it is also a defense.
Scientists have worked hard to find the cause of Alzheimer’s disease. There are other reasons researchers think inflammation causes Alzheimer’s. Studies have found many genes, like CD33, tied to higher Alzheimer’s (AD) risk. Most of these genes play a key role in the immune system and inflammation. Inflammation may raise the risk, but there is still much to learn. After all, inflammation also helps healing, fights infections, and is key to rebuilding tissue.
For the study, researchers enrolled older adults who had brain scans. These people were known to have amyloid beta deposits in the brain. Amyloid beta is a protein tied to AD. Researchers wanted to know why some people with amyloid in the brain go on to get AD while others live on without mental decline. The study enrolled 298 people aged 50 to 90 years. All of them had normal thinking, despite amyloid deposits in the brain. Researchers also tested their blood for nine cytokines to see how the levels tracked with mental decline.
To the researchers’ surprise, people with high levels of a cytokine called interleukin-12 (IL-12) had no real mental decline. Decline was greater in those with lower IL-12 levels. People with high levels of a cytokine called interferon-gamma (IFN-γ) were also less likely to decline.
Researchers think they understand this, even if it seems backward. Higher levels of these cytokines show these people have better immunity against certain germs. They are just better primed to fight certain infections. This fits the theory that early amyloid beta buildup in the brain is a defense against infection. The immune system spins a sticky web to keep infections out of the brain. Sadly, in some people, this shield ends up doing permanent damage to brain cells.
The latest findings suggest that people with higher IL-12 and IFN-γ levels might control infections early. So researchers propose tracking IL-12 and IFN-γ levels in high-risk people. This could serve as a marker to help predict the future, since no such tool exists yet.
The Takeaway
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Frequently asked questions
Does inflammation cause Alzheimer’s disease?
Inflammation is tied to Alzheimer’s, but not in a simple way. More inflammation is tied to a higher risk of dementia and Alzheimer’s. Many genes linked to Alzheimer’s risk, such as CD33, work in the immune system. Yet inflammation is also a defense that fights infection and helps healing. Unchecked, long-running inflammation is the problem. Not every inflammatory response means higher risk.
Does everyone with amyloid plaques get Alzheimer’s?
No. Amyloid and tau proteins build up in Alzheimer’s, but not everyone with amyloid in the brain gets the disease. This study enrolled 298 adults aged 50 to 90 who had amyloid beta deposits on scans yet normal thinking. The goal was to learn why some people go on to get Alzheimer’s while others live on without mental decline.
Is there a test that can predict Alzheimer’s?
Not yet. There is no reliable test to diagnose Alzheimer’s early, and none that predicts how it will progress. People with high IL-12 and IFN-γ levels showed less mental decline. So researchers propose tracking these two cytokines in high-risk people. It may help predict who will get worse.
How can inflammatory proteins protect against cognitive decline?
People with higher IL-12 and IFN-γ seem better primed to fight certain infections. That fits the theory that early amyloid buildup is a defense. The immune system spins a sticky web to keep infections out of the brain. In some people that shield ends up damaging brain cells. Those with higher levels may be able to control infections early.
Dr. Gurpreet Singh Padda, MD, MBA, MHP
