Infections of Chlamydia Pneumoniae and Sars-COV-2 can play a role in Alzheimer’s pathogenesis

A recent review by researchers at Philadelphia (PCC) College (PCC) shows that Chlamydia Pneumoniae (CPN) and Sars-COV-2 infections can play a role in the pathogenesis of Alzheimer’s disease.

Published on the border in the aging of neuroscience, the review emphasizes that both infections increase the levels of substances in the brain called cytokines, especially IL-6 and CCL2, which cause inflammation. This ongoing inflammation can damage the brain cells and can help accelerate the accumulation of harmful proteins associated with Alzheimer’s.

The review shows that CPN and Sars-COV-2 can invade the central nervous system both through blood brain barrier and the most important olfactory pathway, which is responsible for our sense of odor. The olfactory system is lined with a specialized neuroepithelium that can serve as a point of entry for pathogens in the brain. After the initial infection, these germs can travel along the olfactory nerve, eventually reaching the olfactory bulbs of the brain, which are associated with areas of the brain for memory and knowledge. This route is particularly important as the loss of odor is an early symptom in both COVID-19 and Alzheimer’s disease.

The research examined peer-to-COV-COV compounds with Alzheimer’s peer rating studies, in combination with specific genetic risk factors such as APOEE4, biomarkers (IL-6, CCL2, NRP1) and structural and functional aspects of infection and neuros. PCC researchers recorded that people who carry this gene variant seem to be more sensitive to both CPN and Sars-COV-2 infections, possibly enhancing the risk of disease development.

“These findings bring us a step closer to understanding the complex interactions between infections and Alzheimer’s disease,“Brian J. Balin of PCC, PhD, Professor of Neuroscience and Neuropathology and Director of the Center for Aging Disorders (CCDA), who co-author of the report.”As we continue to learn more about the role played by infectious factors in the development of this disease, we hope to create new ways of prevention and treatment. “

Balin and his team have dedicated more than two decades working in the assumption that infectious agents could be a boost to the process that causes the accumulation of amyloid and Tau accumulation, which are key indicators of Alzheimer’s disease. More recently, it has helped to consolidate PCCE’s Pathobiome Research Center to further examine links between infectious processes and other chronic disorders other than Alzheimer’s disease.