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According to scientists, a gum disease virus plays a "central role" in the development of Alzheimer's disease.
New evidence that infectious bacteria are driving Alzheimer's progression could potentially transform current thinking about how the disease should be treated.
Porphyromonas gingivalis is one of the leading causes of gum disease and tooth loss in humans, and has also been badociated with arterial damage.
It has already been suggested that this could play a role in Alzheimer's disease, but the latest study by an international team of scientists led by the United States seems to put this link out of the question.
The researchers made this discovery after badyzing the brain tissue, cerebrospinal fluid and saliva of dead or living patients with diagnosed or suspected Alzheimer's disease.
They discovered traces of toxic enzymes, called gingipains, released by P. gingivalis, as well as DNA from the bacteria.
In addition, it was found that the virus spread from the mouth to the mouse brain.
Animal tests have confirmed that gingipain enzymes destroy neurons in the brain.
However, there was also good news. The scientists tested drugs blocking the gingipains and discovered that they were able to stop neurodegeneration.
A drug, administered to mice in food, effectively treated P. gingivalis brain infections and prevented the loss of memory neurons.
The team has now developed a new drug, COR388, which better penetrates the central nervous system and could form the basis of a human treatment for Alzheimer's disease.
A large-scale clinical trial involving drug delivery to patients with mild-to-moderate Alzheimer's disease is planned for later this year.
Dr. Stephen Dominy, one of the authors of the study and co-founder of the American company Cortexyme, who developed the COR388, said, "The infectious agents have already been involved in the development and progression of Alzheimer's disease, but nothing has proven that this is the case. convincing.
"Now, for the first time, we have strong evidence linking the Gram-negative Pg (P. gingivalis) intracellular pathogen to the Alzheimer's Pathogenesis, while demonstrating the potential of the disease." 39, a clbad of small molecule therapies to change the trajectory of the disease. "
The results are published in the latest issue of Science Advances.
Scientists tested more than 50 brain tissue samples and found that 96% of them contained one type of gingipain enzyme and 91% another.
Additional DNA tests revealed the hmuY gene of P. gingivalis in three brains of deceased Alzheimer's patients.
The gene was also found in cerebrospinal fluid in seven out of ten living patients diagnosed with Alzheimer's disease.
Saliva samples from 10 patients suspected of having Alzheimer's disease were all positive for the P. gingivalis gene.
Studies in mice have shown that blocking gingipaines effectively protects the hippocampus, a critical brain part of memory, from P. gingivalis infection.
It has also reduced inflammation and levels of beta-amyloid, a brain molecule strongly linked to Alzheimer's disease.
By writing in the journal, the scientists concluded, "The results of this study prove that P. gingivalis and gingipains in the brain play a central role in the pathogenesis (development) of Alzheimer's disease, providing a new conceptual framework for the disease. treatment."
Bacteria could enter the brain by infecting cells in the immune system or spreading through the cranial nerves through the head and jaw, the researchers said.
Laboratory tests have shown that gingipain enzymes can cause entanglements of tau – protein nodes in neurons thought to be responsible for the damage caused by Alzheimer 's disease.
The research also confirmed the controversial idea that beta-amyloid peptide would actually be part of the brain's antimicrobial defense system, the team said.
It was thought that infection with P. gingivalis resulted in high levels of beta-amyloid that eventually became toxic.
According to research, traditional broad-spectrum antibiotics are likely to be ineffective against P. gingivalis in the brain. In laboratory experiments, antibiotics did not prevent P. gingivalis-induced cell death.
It has also been shown that the bug is rapidly developing resistance to the broad-spectrum antibiotic, moxifloxacin, but not to COR388.
Dr. David Reynolds, Scientific Director of Alzheimer's Research UK, noted that Alzheimer's disease is likely to have several causes, including a bacterium, a gum disease.
He added, "Maintaining good dental health is an important part of a healthy lifestyle. Although we do not yet know how much this can affect our risk of dementia, the presence of a single type of bacteria is extremely unlikely. the only cause of the condition. "
According to the British Dental Association (BDA), gum disease affects about 45% of the British population.
Many types of bacteria contributed to gum disease, but P. gingivalis was one of the most important.
Professor Damien Walmsley, BDA's Scientific Advisor, said, "This study is a reminder that oral health can not remain an additional option in our health services.
"Everyone's lives can be improved through regular appointments and good oral hygiene, reducing the bacterial load never before in our mouths to a level that is unlikely to cause tooth decay, gum disease, or loss of health." teeth. "
Dr. James Pickett, head of research at the Alzheimer Society, said, "The lab work suggests that this infection could cause brain cell damage, but there is no obvious evidence that it can cause these lesions in humans or cause Alzheimer's disease. .
"The success of this new drug depends on the fact that the infection really plays an important role in Alzheimer's disease.
"It is important to continue in this direction because there has been no new drug against dementia in 15 years. The upcoming clinical trial will be a crucial test to determine whether it may be a potential treatment for Alzheimer's. "
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