Amyloid plaques can be removed from neurons
Has the way to cure Alzheimer's disease finally been found?
Live systemsResearchers from the Mayo Clinic in the USA recently reported a revolutionary discovery, which, in their opinion, should soon lead to the development of an effective method of treating patients suffering from Alzheimer's disease.
Scientists have managed to remove beta-amyloid crystals from the brains of experimental animals with Alzheimer's disease, the accumulation of which in nerve cells is the cause of the development of the disease.
It was found that when interleukin-6 (IL-6) is exposed to microglial cells, beta-amyloid crystals are removed from neurons. The work was carried out on mice with induced Alzheimer's disease. "Our work demonstrates that the impact on immune mechanisms can become a new approach to the treatment of patients suffering from this severe neurodegenerative disease," said Pritam Das, one of the lead authors of the study.
Microglia are a specialized class of glial cells of the central nervous system, which are phagocytes that destroy infectious agents and destroy nerve cells. They originate from blood monocytes (descendants of a blood stem cell), that is, they are characterized by mesodermal origin. Microglial cells are activated during the inflammatory process.
In their experiments, the researchers wanted to prove that the activation of microglia in the brain with the help of the pro-inflammatory cytokine IL-6 should increase the inflammatory process and worsen the course of the disease, but as a result, an unexpected discovery was made. Das and his colleagues believed that microglial cells "will try to remove beta-amyloid crystals from neurons, but they will not be able to do this, and they will only increase the inflammatory response in the brain." To their surprise, microglial cells were able to successfully remove beta-amyloid crystals from the nervous tissue.
The experiments were carried out both on adult animals with already developed Alzheimer's disease, and on newborn mice with a genetic defect that leads to the accumulation of beta-amyloid in brain cells. The IL-6 transgen was embedded in the DNA of experimental animals, thanks to which increased production of this cytokine occurred in the nervous tissue. In both adult and newborn animals, increased production of IL-6 in the brain led to the purification of neurons from beta-amyloid and easing the course of the disease.
"This model is very close to human pathology, and the results give us hope for the development of an effective treatment for Alzheimer's disease," commented Professor Gerald Weissmann, editor–in–chief of The FASEB Journal, "this study is another argument in favor of the fact that experimental biology is the best approach to solving problems with which we meet in an aging population."
Original article: Chakrabarty P. et al. Massive gliosis induced by interleukin-6 suppresses A deposition in vivo: evidence against inflammation as a driving force for amyloid deposition. The FASEB Journal, 2009.
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