The study, led by Prof. Ilana Gouzes from Tel Aviv University with the participation of other researchers from Tel Aviv, Ben Gurion and Australia, was recently published in the journal Schizophrenia Research: Molecular Psychiatry from Nature
A new study from Tel Aviv University found a connection between the autophagy mechanism (autophagy, "self-digestion"), which is responsible for ingesting, breaking down and eliminating harmful substances within the living cell, and the disease of schizophrenia - and offers a new direction for the diagnosis and treatment of the disease.
The study, which was published a few days ago in the prestigious journal Molecular Psychiatry from the Nature group, was conducted by Prof. Ilana Gouzes, PhD students Avia Mernlander-Wagner, Anna Malshekwitz and Ze'ev Shemer from Tel Aviv University, in collaboration with Prof. Galila Agam and Prof. Yosef Levin from Ben-Gurion University in the Negev, and Prof. Brian Dean, Director of the Brain Bank in Victoria, Australia.
"The living cell has defense mechanisms against damage and death, one of the main processes in the living cell is the process of autophagy ("self-eating"), explains Prof. Ilana Guzes, "the process of autophagy leads to the breakdown of proteins, fats and other substances that are not used and are not effective. The breakdown mechanism into important raw materials preserves and increases cell vitality. Many studies show that a decrease in the function of the autophagy process significantly decreases the vitality of the cell and its ability to deal with stressful situations. "A malfunction in the autophagy mechanism will cause the accumulation of harmful substances in the cell. A direct link was found between cell death and dysfunction of this mechanism.
"Many studies point to a connection between aging processes, and between degenerative diseases such as Alzheimer's disease, Parkinson's disease and ALS disease, and even cancer, with the dysfunction of the autophagy process. Our study is the first to indicate a clear connection between the expression of proteins that play a central role in the autophagy process and the disease of schizophrenia. The drugs currently given to schizophrenia patients mainly focus on changes in nerve conduction. Our research offers new targets for drug development for schizophrenia that may be more effective than existing treatment."
In the new study, conducted in a post-mortem examination of 24 brains - 12 healthy brains and 12 brains of schizophrenia patients - it was found that the protein beclin 1, which plays a central role in the autophagy process, is deficiently expressed in schizophrenia patients. It should be noted that the decrease in expression, approximately 40% less than in the control group, was measured in the hippocampus, an important area of the brain responsible for learning and memory processes. The decrease in expression was unique to the brain cells and was not found in the blood cells.
"These biochemical changes in the brain open the door to new approaches to understanding and treating the disease," says Prof. Gozes. "We also tested blood cells from living patients, but we found no change in the expression of beclin 1 in their white blood cells. This is, therefore, a unique deficit for the brain."
beclin 1 is not the only protein that changes in the brain of the patient suffering from schizophrenia. In the past, Prof. Guzes' laboratory discovered a protein essential for the creation of the brain, and gave it the name Activity-dependent neuroprotective protein (ADNP). Later, Prof. Guzes showed that the ADNP protein has a twin brother called ADNP2, the ratio of which is different in the hippocampus of schizophrenia patients. But unlike the expression of beclin 1, the expression of ADNP and ADNP2 does increase in the white blood cells of schizophrenia patients, and could possibly be a marker for the disease.
When Prof. Guzes and her team examined proteins that bind to ADNP, they found a link to another protein that plays a role in the autophagy mechanism: a protein called Light Chain 3, or LC3. "Hence, both the change in beclin 1 and the change in ADNP are related to the deregulation of the autophagy process in the brain of a schizophrenic patient," explains Prof. Gouzes. "The change in the expression of the proteins ADNP and ADNP2 is also evident in the white blood cells - especially at the beginning of the disease, and perhaps the blood cells are trying to protect the brain from the disease with the help of ADNP. From a scientific point of view, we have identified a new biological mechanism for schizophrenia, which opens the door to both new diagnostic methods and the development of innovative drugs."
5 תגובות
What is the problem with researchers? They draw conclusions long before they really understand what they have seen in the research
It is more likely to think that what they discovered is the result of schizophrenia which causes many other disorders (including eating disorders, etc.). And these cause effects.
What is more likely is that this research is trying to start brainwashing in the direction of selling drugs.
I think the glass in the picture is trying to represent manic depression and not schizophrenia.
At the end you will be able to choose whether to be more creative or more "square".
This is the first time I read about a demonstrable and measurable connection between the disease and changes in the brain.