Dr. Noa Bergman explains what causes Alzheimer's, is there a way to prevent the disease, and how to treat someone who is already ill (Walla system!)
By 2050, the number of Alzheimer's patients worldwide is expected to reach approximately 135 million people.
The need for effective treatment is increasing, but despite the knowledge that the disease is associated with mitochondrial dysfunction, drug research has not yet focused on this area.
Now, researchers from Ben-Gurion University of the Negev offer an innovative approach to treating the disease, by targeting the VDAC1 protein, which is the gatekeeper of the mitochondria and controls metabolism.
Their new study was published in the journal Translational Neurodegeneration.
Alzheimer's disease is characterized by severe impairment of memory and cognitive deficits, and it currently affects about 50 million people worldwide and about 10 million new diagnoses are received every year.
Significant evidence pointed to an impairment of the metabolic mechanism in Alzheimer's patients that develops several decades before the onset of dementia and deterioration of cognitive function.
About 10 million new Alzheimer's diagnoses are received every year (Photo: ShutterStock)
Reduced metabolism is caused by a dysfunction of the mitochondria, which is responsible for producing most of the energy in the cell, but is also involved in cell death, inflammation and the immune response.
Therefore, scientists from the National Institute of Biotechnology at Ben-Gurion University of the Negev under the leadership of Prof. Verda Shoshan-Barmetz in collaboration with Prof. Shira Kanaf, Prof. Alon Monsongo and Prof. Noga Vardi from the University of Pennsylvania, studied the dysfunction of the mitochondria in Alzheimer's disease in laboratory mice and tested a possible treatment .
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The research focused on the VDAC1 protein that controls mitochondrial activity and controls cell life and death.
Prof. Varda Shoshan-Brametz's research in the past indicated that an increase in the amount of VDAC1 protein in the cell leads to its organization in a structure centered on a large canal through which proteins that cause cell death and mitochondrial DNA, which leads to the development of inflammation, exit. Moreover, Prof. Varda Shoshan-Brametz showed an increase in the amount of
VDAC1 In diseases of the heart, intestines (colitis), autoimmune diseases such as lupus and others. Here, the researchers showed that the protein is also produced in huge quantities in the brain of a mouse with Alzheimer's and is concentrated in the nerve cells around the phlegm, cells that show a decrease in metabolic activity and in proteins related to neural activity.
"An innovative approach that can be used as a preventive treatment"
In response to all of these, in the laboratory of Prof. Shushan-Brametz, a small molecule, VBIT-4, was developed, which binds to the VDAC1 protein and prevents its organization into the large canal and therefore prevents the changes associated with Alzheimer's.
The molecule prevents symptoms such as the death of nerve cells, inflammation, metabolic dysfunction as well as the damage to other brain cells (such as the astrocytes and microglia that are important for normal brain function).
Furthermore, the treatment was also able to prevent a decline in cognitive skills such as learning and memory.
"The molecule we developed presents an innovative approach to the treatment of Alzheimer's disease and can even be used as a preventive treatment," noted the lead researcher Prof. Verda Shushan-Brametz.
"It is interesting to note that protection against Alzheimer's pathology was obtained by the new molecule without a significant reduction in the amount of plaques that accumulate in the brains of patients and are considered the main causes of Alzheimer's."
These findings together with the data indicating the failure of hundreds of clinical trials based on reducing the amount of plaques, contradict the hypothesis that these proteins are the main cause of the disease.
In this study, other factors are presented as a target site such as improving metabolism, preventing cell death and inflammation, which may change the prevailing opinion so far about the primary cause of Alzheimer's.
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