Researchers say it is still a mystery whether inflammation is a result of having Alzheimer's disease or whether the inflammatory process plays a role in its development. It is probable that inflammation can be a cause and effect of the debilitating brain disorder.
Since the late 1980s, various studies have suggested chronic inflammation found in Alzheimer’s hastens the disease process, and may even be a disease trigger.
Professor Julie Williams, of the Genetic and Environmental Risk in Alzheimer's Disease Consortium at Cardiff University, has said: "We have long known that inflammation is present in the brains of Alzheimer’s patients. And the mainstream research community is warming to the idea that inflammation is an important target to halt or reverse Alzheimer’s progression. But we still don’t know exactly what role neuroinflammation plays in the disease. Is it a malicious driver of Alzheimer’s? Or perhaps it is an inconsequential byproduct of the brain cell damage and death common in the disease. It could also be a beneficial response that is activated to repair or clear away damage. Like most things in biology, the answer is complicated, but more and more research suggests that inflammation plays a very active and early role in the development of Alzheimer’s."
Typically, inflammation is in the body to limit the invasion of foreign bacteria or viruses or parasites, and once these are removed, the inflammation is resolved by anti-inflammatory mechanisms. However, in the Alzheimer’s brain, there is the constant detection of the ongoing amyloid beta protein accumulation, which does not allow the inflammation to resolve.
Immune cells in the brain, called microglia, are normally present to clean up infections, which in turn, protect the brain from inflammation. Microglia constantly patrol the brain, so to speak, looking for signs of infection or inflammation caused by toxic proteins such as beta-amyloid and anything else that may damage the brain cells, or neurons.
Microglia recognize the amyloid plaques of Alzheimer's as unwanted and attack them as they would attack an infection. When these immune cells are disturbed by the buildup of too much amyloid beta protein in the brain, they become aggravated, causing the microglia to release too much protein. The release of excessive protein by microglia can cause a breakdown at the synapses, or connections between the nerve cells in the brain. Synapses allow communication between neurons and make it possible to create and recall memories. And, when these connections are damaged, the losses result in a cognitive decline, one of the key features of Alzheimer's disease.
Chronic microglial activation remains an important component of neurogenerative diseases like Alzheimer's and dementia, and this component possibly contributes to brain dysfunction, injury and inflammation leading to disease progression. The inflammation both degenerates brain tissue and increases amyloid beta, the hallmark of Alzheimer’s disease.
Research continues to target specific elements of inflammation which could be useful in treating or preventing the disease.
Questions about Alzheimer's disease or related disorders can be sent to Dana Territo, the Memory Whisperer, owner of Dana Territo Consulting, LLC, at email@example.com.