Although Alzheimer's disease is associated with mitochondrial dysfunction, there is currently no
VDAC1 plays a critical role in the death processcells mediated by mitochondria. Therefore, as a potential target, scientists focused on mitochondrial dysfunction in a mouse model of Alzheimer's disease.
Research has shown that an increase in the numberVDAC1 protein in the cell leads to its organization in the form of a ring with a large channel through which death factor proteins and mitochondrial DNA exit, causing cell death and an immune response, respectively. Also, a high increase in VDAC1 levels was found in heart diseases, intestinal diseases (Crohn's disease), autoimmune diseases (lupus) and others. Scientists have shown that the protein is produced in huge quantities in the brain of a mouse model of AD.
Researchers have developed a small moleculeVBIT-4, which binds to VDAC1 and prevents pathophysiological changes associated with AD. VBIT-4 crosses the blood-brain barrier and prevents pathophysiological changes associated with Alzheimer's disease, such as neuronal death, neuroinflammation and neurometabolic dysfunction. In addition, the molecule induced a neuroprotective phenotype in astrocytes and microglia.
The treatment didn't just protect the brainfrom degeneration, but also promoted healthy growth and normal functioning of neurons. The therapy also prevented the decline in cognitive skills.
Interestingly, protective effects were achieved withoutsignificant reduction of tau or amyloid (Aβ) plaques. They are believed to be the cause of Alzheimer's disease. The study found that the Aβ cascade hypothesis does not explain the underlying cause of Alzheimer's disease.
“Targeting VDAC1 with a new molecule that"We have developed an innovative approach to the treatment of Alzheimer's disease and will be useful as a preventive treatment," the scientists conclude. Thus, scientists not only refuted the hypothesis about the appearance of AD, but also proposed a fundamentally new treatment.
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On the cover: MRI images of progressive Alzheimer's disease with extensive loss of brain tissue
Copyright: Av Tetz V, Tetz G/J Med Case Rep (2016). Lisens: Falt i det fri (Public domain)