Immune genes change in the blood of Alzheimer's patients

A new study from Northwestern Medicine reveals epigenetic changes in the immune system in the blood of Alzheimer's patients. This means that the patient's behavior or environment has caused changes that affect how the gene works.

Many of these have changed immune gene The same things that increase an individual's risk of Alzheimer's disease. Northwestern scientists theorize that the cause may be a past viral infection. environmental pollutants or other lifestyle factors or behaviors.

“These findings may implicate the peripheral immune response in Alzheimer's disease risk,” said lead researcher David Gate, assistant professor of neurology at Northwestern University Feinberg School of Medicine. “These changes brain pathology Or whether they promote disease. ”

The study was published on February 9th. neuron.

Previous research has shown that many of the mutated genes that put people at higher risk for Alzheimer's disease immune system. However, because Alzheimer's disease is a brain disease, scientists were primarily studying the brain's central immune system. They have largely ignored the immune system in the blood, also known as the peripheral immune system.

Gate decided to study blood. He and his colleagues found that all types of immune cells in Alzheimer's patients epigenetic changesindicated by open chromatin. Chromatin is the packaging of DNA within cells. When chromatin is open or exposed, a cell's genome is more susceptible to changes.

Gates then looked at which genes were more open in these immune cells. He found that a receptor (CXCR3) on T cells was further exposed. Gates believes that CXCR3 acts like an antenna on T cells, allowing them to enter the brain. T cells do not normally enter the brain because they can cause inflammation.

“The brain is sending out a signal that it is damaged, and the T cells are homing towards that signal with their antennae, CXCR3,” Gates said.

“T cells can be very toxic in the brain, but we also don't know if these cells are trying to repair brain damage,” Gate said.

Gate also discovered epigenetic changes in inflammatory proteins. white blood cells called monocytes.

“Taken together, these findings demonstrate profound changes in immune function in patients with Alzheimer's disease,” Gate said. “Environmental factors, such as pollutants and infections that a person suffers from during their lifetime, can trigger these epigenetic changes.”

This discovery uncovers several genes that could serve as potential therapeutic targets for manipulating the peripheral immune system. The next step in research is preclinical studies using in vitro culture systems and animal models to test these targets.

Other Northwestern authors include Abhirami Ramakrishnan, Natalie Peele, Brooke Simonton, Milan Parikh, Ziyang Zhang, Victoria Teleglowa, and Lin van Orst.

The title of the paper is “Epigenetic dysregulation in peripheral immunity in Alzheimer's disease.”

For more information:
Abhirami Ramakrishnan et al, Epigenetic dysregulation in peripheral immunity in Alzheimer's disease, neuron (2024). DOI: 10.1016/j.neuron.2024.01.013

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northwestern university

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