Researchers from the University of Colorado found that Protein inhibiting MDM2 With the help of nutlin, the destruction of synapses during Alzheimer's disease. Details about the new treatment method.
According to researchers from Medical campus ANSHUTZ at Colorado Universityinhibiting the key protein can prevent destruction synapses And dendritic cellsthat is often observed with Alzheimer's disease.
Using neurons of rodents, scientists have found that the effect on the protein MDM2 With the help of experimental antitumor drug called Nutlin Stops the formation of neurotoxic amyloid-β peptideswhich cause accumulations at Alzheimer's disease.
“Cognitive disorders associated with Alzheimer's disease are associated with the loss of dendritic cells and exciting synapses, especially in the hippocampus”– said the leader of the research professor Mark Dell'akvadeputy head of the department pharmacology Medical School of the University of Colorado.
Each neuron has many dendrites – short branching processes of cells. These structures form a network through which neuron receives signals from other cells. These impulses reach dendrites each nerve cell from Neurites (one or more) other nerve cells. Thus, nerve cells are connected, branched and interact with each other, forming groups to perform their functions – transmitting stimuli from periphery to center (brain) and vice versa. At the ends dendrites Located Presenaptic nodes And Sinapsesthrough which the cell receives or transmits signals.
Dell'akva noted that the natural reduction of excessive dendritic synapses to some extent is the norm, but with Alzheimer's disease This process can accelerate abnormally, causing a loss of memory and ability to learning.
“When this MDM2 protein is activated inadequate, this leads to the“ pruning ”of synapses in the presence of amyloid-β, the main component of amyloid plaques found in the brain of Alzheimer's disease. When we used the drug that inhibits the MDM2 in neurons, it completely blocked the loss of dendrites caused by amyloid β. So the inhibition of this protein is clearly working “.
Dell'akva, who is also the director Center for Neurotechnology at Medical School of the Universityemphasized that most studies on the treatment of this disease are usually focused on removing Beta-amyloid plaques From the brain.
“There are questions about whether therapy aimed at amyloid is the end point of treatment of Alzheimer's disease. Even if someone can afford a high cost, the effectiveness is not guaranteed. We say that you can intervene in the process, blocking some effects of beta-amyloid. And this applies to exposure to MDM2 “.
The next step is to determine whether scientists can stop the progression of the disease in animal models. If this succeeds, future tests may include clinical tests in public. Preparations aimed at MDM2clinical trials for treatment have already been developed and undergoes Cancerbut require approval FDA.
The results of the study are published in a medical journal Eneuro.
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