ISLAMABAD, Feb 17 (Online): With rates of Alzheimer\u2019s disease expected to riseTrusted Source and still no cure for this type of dementia, finding new ways to treat this disease has been at the forefront of research over the past few years.
\nAdding to this research is a new study from Northwestern University Feinberg School of Medicine. The findings recently published in the journal NeuronTrusted Source found that immune cells in the blood of people with Alzheimer\u2019s disease are epigenetically alteredTrusted Source.<\/p>\n
This alteration, the researchers say, is potentially caused by a previous viral infection, environmental pollutants, or other lifestyle factors.
\nThe research revealed several genes that may be therapeutic targets for manipulating the body\u2019s peripheral immune systemTrusted Source.
\nWhat is the peripheral immune system?
\nThe body\u2019s immune system can be considered as comprising two parts \u2014 the central immune system and the peripheral immune system, a term used to describe immune responses that happen outside the brain.<\/p>\n
The peripheral immune system includes circulating white blood cells that detect antigens, such as bacteria or viruses, when they enter the body. This part of the immune system acts as the first wave of attack against any foreign substance.
\nAccording to Dr. David Gate, assistant professor of neurology at Northwestern University Feinberg School of Medicine and senior and corresponding author on this study, there is mounting evidence that the peripheral immune system plays a role in Alzheimer\u2019s disease.
\n\u201cIn recent years, we have shown that immune cells of the cerebrospinal fluid \u2014 a fluid that flows in and around the brain \u2014 are clonally expanded and activated,\u201d Dr. Gate told Medical News Today. \u201cThis means that they have previously responded to some type of immune stimulus.\u201d<\/p>\n
Previous researchTrusted Source has connected the peripheral immune system to neurodegenerative diseases, and studiesTrusted Source have shown an association between types of peripheral immune cells and cognition, brain structure, and Alzheimer\u2019s disease pathology.
\nHow epigenetics may play a role in Alzheimer\u2019s disease
\nFor this study, Dr. Gate said the team wanted to find out whether there might be epigenetic changes within the immune system of Alzheimer\u2019s disease patients that might promote the trafficking of these changes to the cerebrospinal fluid and the brain.<\/p>\n
\u201cEpigenetics essentially reflects changes to our DNA that have occurred in the past,\u201d he explained. \u201cThere are many influences on epigenetics, such as the environment, pollutants, viral infections, lifestyle factors, and behaviors. It is possible that these influences work in concert, or in isolation, to promote inflammation that puts one at risk of developing Alzheimer\u2019s disease.\u201d
\nDr. Gate and his team examined immune cells from peripheral blood samples taken from people with Alzheimer\u2019s disease. When compared to healthy controls, researchers found that every immune cell type in the participants with Alzheimer\u2019s disease had epigenetic changes indicated by open chromatinTrusted Source.<\/p>\n
Additionally, scientists looked for which genes were more open in the immune cells and found more exposure in the protein CXCR3Trusted Source on T cellsTrusted Source.
\n\u201cEpigenetic changes alter the way our genes are translated into proteins,\u201d Dr. Gate explained. \u201cIn this study, we observed an epigenetic change in a gene that encodes the protein CXCR3. CXCR3 is a signal receptor on the surface of immune cells called T cells. This receptor essentially serves as an antenna that we believe allows them to traffic signals put out by the Alzheimer\u2019s brain.\u201d<\/p>\n
Researchers also found epigenetic changes in a type of white blood cell called monocytesTrusted Source.
\n\u201cMonocytes are very important to immune defense. They secrete inflammatory proteins that protect your body in the case of infection. In this study, we found that there are epigenetic changes to genes that encode these inflammatory proteins. This is significant because it could signal that Alzheimer\u2019s disease patients have a more pronounced pro-inflammatory immune system.\u201d<\/p>\n
\u2013 Dr. David Gate
\nViral infections may increase Alzheimer\u2019s risk
\nAs epigenetics only provides a snapshot into the past, Dr. Gate said we can only speculate on what might have caused these discovered epigenetic changes.<\/p>\n
\u201cHowever, in the past decade, we have grown to appreciate the fact that viral infections are a risk factorTrusted Source for the development of dementias like Alzheimer\u2019s disease,\u201d he continued.
\n\u201cWhile our data do not provide evidence that epigenetic changes in Alzheimer\u2019s disease patients\u2019 immune systems were caused by viral infections, this is certainly a tantalizing possibility. In this scenario, viral infections promote inflammatory responses over the course of one\u2019s life that promote Alzheimer\u2019s disease risk via mechanisms that we do not yet understand,\u201d suggested Dr. Gate.
\n\u201cOur ultimate goal is to design immune cell therapies for Alzheimer\u2019s disease,\u201d Dr. Gate added. \u201cUsing information from this study, we can potentially target the genes that harbor epigenetic changes.\u201d<\/p>\n
\u2018Implications in prevention and treatment of Alzheimer\u2019s\u2019
\nAfter reviewing this study, Dr. Manisha Parulekar, chief of the Division of Geriatrics at Hackensack University Medical Center in New Jersey, not involved in the research, told MNT she was not surprised by its results.
\n\u201cBasically, it reinforces the idea that the patient\u2019s behavior or environment has caused changes that affect the way their genes work,\u201d Dr. Parulekar explained. \u201cMany of these altered immune genes are the very same ones that increase an individual\u2019s risk for Alzheimer\u2019s.\u201d
\n\u201cAlzheimer\u2019s disease is known to have complex pathophysiology, possibly involving multiple genes in combination [with] lifestyle, environmental, and other risk factors. Reading this new article, I am excited to see more evidence of changes in immune cells with changes in genes that were attributed to Alzheimer\u2019s disease. The advancement in this science will likely have implications in [the] prevention and treatment of Alzheimer\u2019s disease.\u201d<\/p>\n
\u2013 Dr. Manisha Parulekar
\nMNT also spoke with Dr. Karen D. Sullivan, a board-certified neuropsychologist, owner of the I CARE FOR YOUR BRAIN program, and Reid Healthcare Transformation Fellow at FirstHealth in Pinehurst, NC, about this study.
\nDr. Sullivan said that as we do not know much about the peripheral immune system in Alzheimer\u2019s disease, this study is a novel contribution to our understanding of a very complex, multi-faceted neurodegenerative disease.<\/p>\n
\u201cThe main question I have is the directionality here,\u201d she continued. \u201cIs the peripheral inflammatory response in Alzheimer\u2019s disease a cause or effect? The best thing I take away is that we may have a new therapeutic target in Alzheimer\u2019s disease: restricting peripheral inflammation.\u201d
\n\u201cWe would need to see these results replicated in larger sample sizes and to more deeply understand their relationships to the functional decline of Alzheimer\u2019s disease,\u201d Dr. Sullivan added.<\/p>\n","protected":false},"excerpt":{"rendered":"
ISLAMABAD, Feb 17 (Online): With rates of Alzheimer\u2019s disease expected to riseTrusted Source and still no cure for this type of dementia, finding new ways to treat this disease has been at the forefront of research over the past few years. Adding to this research […]<\/p>\n
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