Unveiling the Epigenetic Alterations in Alzheimer's Patients: A Potential Link Between the Immune System and Disease Risk

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Zara Nwosu
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Unveiling the Epigenetic Alterations in Alzheimer's Patients: A Potential Link Between the Immune System and Disease Risk

Unravelling the Mysteries of Alzheimer's Disease

A recent breakthrough study by Northwestern Medicine takes us a step closer to understanding the complex and multifactorial nature of Alzheimer's disease. The study has discovered significant alterations in the immune system of Alzheimer's patients, suggesting a potential link between behavior, environment, gene function, and disease risk. The findings of this study have been published in the esteemed scientific journal, Neuron.

Alzheimer's and the Immune System: The Epigenetic Perspective

David Gate, the lead investigator of the study, theorizes that various factors such as viral infections, environmental pollutants, and lifestyle factors may contribute to these changes. It is suggested that these factors can trigger epigenetic alterations in the immune system, implicating the peripheral immune response in Alzheimer's disease risk. Epigenetic changes do not alter the DNA sequence but can affect gene function, impacting how cells 'read' genes.

The focus of this study was the immune system in the blood. The researchers discovered that every type of immune cell in Alzheimer's patients exhibited epigenetic changes. Open chromatin was observed, indicating a vulnerability to alterations. Chromatin is the material in the cell nucleus that encompasses the DNA and proteins, with 'open' chromatin regions being more accessible for transcription and thus, more vulnerable to changes.

Unearthing Potential Therapeutic Targets

One of the most significant findings of this study is the identification of several genes that may serve as potential therapeutic targets for manipulating the peripheral immune system. Among these, the CXCR3 receptor in T cells has been highlighted. T cells are vital components of our immune system, and the CXCR3 receptor plays a significant role in their function.

The research also identified epigenetic changes in monocytes that are dependent on the apolipoprotein E genotype. Monocytes are a type of white blood cell that can develop into macrophages and dendritic cells to fight against infection. The apolipoprotein E is a major cholesterol carrier that supports lipid transport and injury repair in the brain. Alterations in this gene are known to influence Alzheimer's disease risk.

Implications of the Study and Future Directions

The findings of this study provide valuable insights into the significant alteration in immune function in Alzheimer's patients. By implicating the peripheral immune system in the disease risk, the study opens new avenues for exploring therapeutic interventions. Manipulating the peripheral immune system could potentially lead to the development of novel treatments for Alzheimer's disease.

This ground-breaking research has been generously supported by National Institute of Neurological Disorders and Stroke grant NS112458 and National Institute on Aging grant AG078713, both of the National Institutes of Health, Bright Focus Foundation, Alzheimer’s Association and Cure Alzheimer’s Fund. The continued support from these organizations will undoubtedly catalyze further research in this area, bringing us closer to finding a cure for Alzheimer's disease.