Experimental drug against Alzheimer's disease
Unstable blood supply disrupts the normal functioning of neurons. Therefore, it is believed that one of the causes of the development of Alzheimer's disease are blood clots, which often form in the blood vessels of the brain of patients with this disease, characterized by memory loss, confusion and loss of cognitive functions.
Rockefeller University researchers working under the guidance of Dr. Sidney Strickland have identified a compound capable of stopping the progression of Alzheimer's disease by blocking the thrombosis process triggered by beta-amyloid.
For more than ten years, the target of practically all drugs being developed for the treatment of Alzheimer's disease has been beta-amyloid, a protein that forms so–called amyloid plaques in brain tissue, which are the "calling card" of the disease. However, when conducting clinical trials, these drugs either do not have the expected effect, or cause serious side effects.
The authors decided to approach the issue from the other side and based the research on the data they had previously obtained, according to which beta-amyloid can interact with a component of the blood coagulation system – fibrinogen. The result is the formation of blood clots that disrupt blood circulation and cause the development of inflammation, leading to the death of neurons.
During the screening of 93,715 compounds, the purpose of which was to identify a molecule capable of preventing the interaction between beta-amyloid and fibrinogen, and subsequent laboratory experiments, the researchers settled on a small synthetic molecule RU-505. This compound is able to penetrate the blood-brain barrier and selectively interact with beta-amyloid without affecting blood clotting.
Testing the effectiveness of RU-505 on a mouse model of Alzheimer's disease has brought promising results. The therapy, which lasted 3 months, reduced the severity of chronic inflammation and significantly improved blood circulation in brain tissue. In addition, the treated animals showed improved results when performing tests to find a way out of the maze.
RU-505 therapy reduces the severity of neuron-damaging chronic inflammation (red)
in the brain tissue of a mouse model of Alzheimer's disease (left) compared
with the condition of the brain tissue of untreated animals (right).
The researchers note that their proposed drug does not provide a complete cure for the disease, but it allows for pronounced improvements. Currently, they are engaged in improving the developed approach, including reducing the toxicity of RU-505, manifested by inflammatory reactions in the injection zone.
Article by H. J. Ahn et al. A novel A-fibrinogen interaction inhibitor rescues altered thrombosis and cognitive decline in Alzheimer's disease mice is published in the Journal of Experimental Medicine.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on the materials of Rockefeller University:
Potential Alzheimer’s drug prevents abnormal blood clots in the brain.
01.07.2014