How the Immune System Could Contribute to Alzheimer’s Disease
The immune system is our last line of defense against invasive organisms and the primary responder to damage within the body. However, for all the good it accomplishes, the immune system can also cause a lot of harm. An impaired immune system may mistakenly attack healthy tissues, as is the case in a group of affiliations called autoimmune diseases (which includes type 1 diabetes, rheumatoid arthritis, psoriasis, and much more).
There are also cases where a normally functioning immune system can cause collateral damage as a side effect of doing its job. Recent research suggests that this scenario may be a driving force in the formation of Alzheimer’s disease.
The Immune System and the Brain
The human immune system is a complex network of pathways, structures, and cells that perform a wide range of protective and healing functions throughout the body. A specialized part of the immune system known as the neuroimmune system takes care of the brain (and spine) separately from the rest of the body. The neuroimmune system is mostly made up of specialized cells called glial cells. There are several types of glial cells and together they perform a collection of important functions. Among their most critical jobs are protecting and repairing the cells that make up the brain (aka neurons).
Microglia are the most active and abundant kind of glial cells in the neuroimmune system. They can also be quite vicious. Microglia belong to a category of immune cells called macrophages, which basically means that they can “eat” other cells. Their main targets are infectious organisms and damaged or unnecessary cells. When microglia are activated by detecting one of their targets they release chemicals that can trigger an inflammatory response.
Inflammation is the term given to our body’s complex reaction to an activated immune system. It usually results in swelling, heat production, and an impairment in functioning at the site of the response. As most of us know, inflammation can be uncomfortable or even painful when experienced in any part of the body. Typically, the experience is worth it due to its short-lived nature and general effectiveness against injuries, infections, and other forms of damage. However, inflammation can become a serious problem when present for a prolonged period of time.
Alzheimer’s and Inflammation
Neuroinflammation is the term used to describe an inflammatory response in the brain, and it could be at least partially responsible for the early progression of Alzheimer’s disease. One of the hallmarks of Alzheimer’s is the abnormal buildup of certain proteins in the brain. A protein called amyloid β (pronounced “beta”) is one of the worst offenders. This protein accumulates into deposits called plaques in the brains of Alzheimer’s patients. Plaques activate the immune system and are targeted by microglia, causing prolonged neuroinflammation in the affected brain areas.
Researchers used to think that inflammation in the brains of Alzheimer’s patients was simply a natural response to the plaques that did not warrant any further investigation. However, in recent decades, it has become apparent that there is nothing simple about the way that the immune system interacts with Alzheimer’s disease. In the early stages of Alzheimer’s, activated microglia may actually be associated with an increase in amyloid β plaques because of the chemicals they release to signal the rest of the immune system. This would create a self-sustaining case of chronic inflammation, where more plaques cause more microglia to activate, which in turn cause more plaques. The brain would then come to suffer damage from the effects of a chronic inflammatory response in combination with a steadily increasing amount of protein deposits.
The Search for New Treatments
Research into the relationship between neuroinflammation and Alzheimer’s disease is relatively new, with many questions left to be answered. One of the more complicated aspects of our current understanding is that, while inflammation appears to cause havoc during the early stages of Alzheimer’s, it may become more beneficial as the disease progresses. This situation must be clarified in order to know when anti-inflammatory medications would be most effective and when they may do more harm than good.
Despite our current lack of knowledge, there is undoubtedly a strong potential for the development of improved treatments and preventative measures to emerge as we come to better understand the link between inflammation and Alzheimer’s disease. Until we can identify and prevent the root causes of this disease and other dementias, the early signs of abnormal psychological decline will often remain our first clue that something is wrong. A self-administered tool like the BrainTest® app is an easy way to monitor the risk, and early detection will give us the most time to explore potential treatments.