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One day it may be possible to use the immune system and force it to fight Alzheimer's disease. A recent study makes us one step closer to being a reality.
The study found new ways to destroy the Alzheimer's plates (pictured here).
is a neurodegenerative condition that affects people in the United States.
About 1 in 10 people over the age of 65 have Alzheimer's disease. Despite the alarming prevalence, there is still no medicine and there is no way to slow down progress.
Precise mechanisms in the case of Alzheimer's disease are not fully understood, but it is known to have a toxic increase in protein called beta-amyloid. With the rise of amyloid plaques, nerve cells start to die.
Over the years, immunity has become a role in this disturbing state. However, it is a complicated and reciprocal link.
For example, the immune system may reduce the progression of Alzheimer's disease by purifying toxic proteins; On the other hand, immune cells can react to amyloid plaques and cause an inflammatory reaction, which in the long run causes more damage to the brain tissue.
The role of microglia
One of the types of immune system that seems to be the key is the type of macrophages that make up the brain's first line of defense. These cells are responsible for cleaning debris, toxins and pathogens in the brain.
However, in Alzheimer's disease microglia does not meet their responsibilities. The dysfunction of these cells can at least partly be responsible for the increase of amyloid plaques in the brain.
Recent research on Alzheimer's disease and immune response has been obtained at the University of Florida in Gainesville. Managed by Paramita Chakrabarty, Ph.D. and Dr. Todd E. Golde led the scientists to be particularly interested in a protein family called Toll-like receptors (TLRs).
TLR sits on the surface of the immune cells; they reveal molecules that come from broken cells or invade pathogens and cause an immune attack.
Researchers found that people with Alzheimer's disease had significantly more TLRs in the brain. This was mainly due to the increased amount of microglia.
Researchers hypothesized that if they separate some TLRs from microglia, they can act as "snail receptors" that reduce the accumulation of amyloid plaques.
Protein-aggregation could be prevented because free-floating TLRs could chew beta-amyloid before it got the chance to blend together. It can also prevent the binding of undesirable protein to microglia and cause harm.
As the team predicted, applying this approach to one TLR subtype, called TLR5, prevents and possibly even changes the formation of amyloid plasters in the Alzheimer's mouse model.
Paradigm shift in Alzheimer's research
According to the authors of the study, this approach marks the "paradigm shift" in Alzheimer's and immune system studies; Instead of introducing "very engineered" antibodies for target amyloid plaques, they use a razor-based approach using naturally occurring protein.
The authors hope that this could create a relatively safe way of treating Alzheimer's disease. Their conclusions were recently published.
The results are exciting, but Chakrabarty recommends caution, saying "This mouse model is well recognized as the main model for deposition of Alcheimer-type amyloidate coating, but it does not collect the entire Alzheimer's neurodegenerative cascade."
"Therefore, in a number of Alzheimer's disease models, the potential impact of soluble TLR5 on inhibition of immune activity and related neurotoxic techniques should be further explored."
"By direct interaction with beta-amyloidroid and beta-amyloidosis in mice, the soluble TLR5 relaxation receptor is a new and potentially safe class of Alzheimer's immunomodulatory agents."
Dr. Todd E. Golde
Using this method to treat people is still a long way to go, but new discoveries create hope. As the burden of Alzheimer's disease is so high among the US population, the disease research sounds fast.
There is no doubt that this new direction will be expanded rapidly.
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