How to incite macrophages on amyloid plaques
Scientists at Yale University, working under the guidance of Dr. Richard Flavell, assumed that blocking the transforming growth factor beta (TGF-beta) involved in the formation of immune responses would contribute to the accumulation of amyloid deposits observed in Alzheimer's disease.
According to the results of earlier studies, patients with Alzheimer's disease are characterized by high levels of transforming growth factor beta, which is a key link in the activation of the immune system response to tissue damage. Some experts suggest that the increase in the level of this compound is an attempt by the body to suppress the inflammatory process caused by the formation of amyloid plaques.
To their surprise, the authors found that in transgenic mice, which are a model of Alzheimer's disease, blocking the activity of transforming growth factor beta using genetic engineering methods eliminated amyloid plaques by 90%.
Amyloid plaques are thought to damage neurons and stimulate an inflammatory response mediated by microglial cells. Theoretically, Alzheimer's disease can be cured by eliminating plaques and suppressing the inflammatory process. The main difficulty in the treatment of this disease is the presence of a blood-brain barrier around the brain that prevents the penetration of therapeutic agents into the brain tissue.
Suppression of TFR-beta activity in mice with Alzheimer's disease improved the ability of mice to perform various tests, including tests to find a way out of the maze, compared with control group animals. In addition, the experimental group of mice had decreased levels of other biomarkers associated with dementia.
The authors claim that blocking the activity of TFR-beta stimulates the movement of peripheral macrophages through the blood-brain barrier, which surround neurons and eliminate amyloid plaques in the brain. If the experimental results are confirmed in clinical trials, doctors will have a new method of combating Alzheimer's disease, which consists in intravenous administration of a drug that directs macrophages to fight amyloid plaques.
Portal "Eternal youth" www.vechnayamolodost.ru based on the materials of ScienceDaily
03.06.2008