COR388 against Alzheimer's disease
Scientists from the UK continue to test the hypothesis of the involvement of oral microflora in the pathogenesis of Alzheimer's disease and confirmed that the use of an experimental antimicrobial drug reduces the concentration of biomarkers of this disease in the cerebrospinal fluid of participants in a phase I clinical trial.
At an international conference dedicated to Alzheimer's disease, the results of a study of a group of 9 people with mild and moderate severity of the disease were presented.
Six patients, whose average age was 72 years, randomly received COR388 for four weeks, which inhibits toxic protease proteins produced by Porphyromonas gingivalis bacteria. The remaining 3 patients received placebo. Bacteria colonize the mouth and gums, have been found in the brain and cerebrospinal fluid in patients with Alzheimer's disease in much larger quantities than in people without this diagnosis.
With the help of conventional antibiotics, it is difficult to completely cure the infection caused by P.gingivalis. The effect of COR388 is based on another mechanism: it neutralizes the harmful effects of bacteria, not killing them, but binding to the proteins they produce. Scientists have suggested that bacterial proteases can act on the cleavage of apolipoprotein E (ApoE) in the cerebrospinal fluid, which in turn leads to a violation of lipid metabolism in the central nervous system and a predisposition to the formation of neurotoxic amyloid beta oligomers. When taking an experimental drug, a decrease in toxic products (in particular, RANTES chemokines) by 30% was noted. There was also an improvement in the cognitive functions of the subjects.
ApoE is known to play a role in Alzheimer's disease: people who have a certain genetic variant of the protein have a greater tendency to develop neurodegenerative disease.
The results obtained do not yet prove that the drug prevents the development of dementia, but at least makes this approach interesting for the scientific community.
The microbiological approach contradicts the usual theories about the development of Alzheimer's disease. It is believed that this condition is caused by the accumulation of toxic protein beta-amyloid plaques in the brain, but numerous trials of treatments that block the accumulation of beta-amyloid have failed to stop the progression of the disease, and it is now believed that the protein is a side effect of Alzheimer's disease, and not the main cause.
Although at the moment many people are skeptical about the hypotheses about the infectious causes of Alzheimer's disease, scientists do not plan to stop research. At the conference, Dr. Detke presented detailed plans for a phase II placebo-controlled clinical trial of COR388 on 570 patients aged 55-80 years with mild to moderate Alzheimer's disease.
Patients will randomly receive a drug or placebo for 48 weeks. The study will monitor patients' cognitive abilities and biomarkers associated with neurodegenerative diseases.
Elena Panasyuk, portal "Eternal youth" http://vechnayamolodost.ru / based on the materials of the AAIC conference