According to a recent Northwestern Medicine research, Alzheimer’s sufferers’ blood has epigenetically changed immune systems. This indicates that alterations in the patients’ behaviour or surroundings have impacted how their genes function.
Numerous of these mutated immune genes also raise a person’s risk of Alzheimer’s disease. Scientists at Northwestern University theorise that a prior virus infection, toxins in the environment, or other aspects of lifestyle and behaviour might be the cause.
It is possible that these findings implicate the peripheral immune response in Alzheimer’s disease risk.
We haven’t yet untangled whether these changes are reflective of brain pathology or whether they precipitate the disease.
Lead investigator David Gate, assistant professor of neurology at Northwestern University Feinberg School of Medicine
The data of the investigation is published in the journal Neuron.
Numerous immune system genes are among the altered genes that increase a person’s chance of developing Alzheimer’s disease, according to an earlier study. But because Alzheimer’s is a brain disease, researchers focused mostly on the brain’s central immune system. The peripheral immune system, found in the blood, has received little attention from them.
Gate chose to examine the blood. He and associates found that all immune cell types in Alzheimer’s patients have open chromatin, a sign of epigenetic modifications. Chromatin is the packing of the DNA within cells. The genome of the cell is susceptible to changes when chromatin is exposed, or open.
Gate then looked at the genes in these immune cells that are more exposed, or more open. He found that the T cells’ CXCR3 receptor was more exposed. According to Gate, T cells’ CXCR3 acts as an antenna to let the cells access the brain. Since T cells have the potential to produce inflammation, they often do not penetrate the brain.
The brain is emitting a signal that it is damaged, and the T cells are homing to that signal by their antenna, CXCR3.
T cells can be very toxic in the brain, but we also don’t know if these cells might be attempting to repair the damage in the brain
David Gate
Gate also found that the inflammatory proteins in monocytes, which are white blood cells, had altered epigenetic modifications.
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Altogether, these findings indicate that immune function in Alzheimer’s patients is significantly altered.
It could be that environmental factors, like pollutants, or infections that a person has in their lifetime cause these epigenetic changes.
David Gate
The results identified a number of genes that might be used as therapeutic targets to influence the peripheral immune system. Preclinical investigations employing animal models and in vitro culture methods to investigate these targets are the next stages of the study.
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Source: Northwestern Now
Journal Reference: Abhirami Ramakrishnan, Natalie Piehl, Brooke Simonton, Milan Parikh, Ziyang Zhang, Victoria Teregulova, Lynn van Olst, David Gate. Epigenetic dysregulation in Alzheimer’s disease peripheral immunity. Neuron, 2024; DOI: https://doi.org/10.1016/j.neuron.2024.01.013
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