Porphyromonas Gingivalis and Alzheimer's disease

Gum disease affects approximately the population. A drug that blocks the main toxins of P. gingivalis enters this year's clinical trials. It could stop and even reverse Alzheimer's disease and eventually give rise to a vaccine.

Dementia, which is currently the fifth leading cause of death worldwide, is a medical mystery as populations age and grow. Dementia accounts for about 70% of these deaths, but its cause is not fully understood.

There is growing evidence that the function of amyloid proteins may be a defense against bacteria, which has inspired recent studies of AD bacteria, particularly those that cause gum disease, which is a known risk of this disease because found after death in the brains of people with the disease. However, it was not clear whether these bacteria were causing the disease or were there through brain damage caused by the disease so far.

Porphyromonas Gingivalis was found to invade and inflamed areas of the brain affected by AD; Gum infections exacerbate symptoms in AD model mice; and it causes brain inflammation similar to Alzheimer's disease, neuronal damage and amyloid plaques in healthy mice.

A cortoxyme discovered the discovery of toxic enzymes for gingipain used by Porphyromonas Gingivalis to feed on human tissue in 96% of the 54 brain samples badyzed, and found the bacteria in the three brains of the disease. Alzheimer whose DNA had been examined. DNA in the human brain and badociated gingipains co-locating with plaques; Gingipains have also been shown to cut tau proteins to kill neurons.

Those who had experienced more severe cognitive decline were found to have higher levels of bacteria and their enzymes. The bacterium has also been found in the cerebrospinal fluid of people living with the disease, suggesting that the technique may provide a diagnostic method.

When Porphyromonas Gingivalis was administered to mice, it resulted in cerebral infection, amyloid production, tau tangles and neuronal lesions in regions and nerves typically affected by AD. It was observed that the administration of previously blocked Gingipan molecules to these mice reduced infections, stopped amyloid production, decreased brain inflammation and saved damaged neurons without developing resistance; Antibiotics that kill Porphyromonas Gingivalis also did, but with less efficacy, and the bacteria developed a rapid resistance.

Some brain samples from individuals without AD also had lower levels of Porphyromonas Gingivalis and accumulations of protein. Amyloid and tau proteins can accumulate in the brain for 10 to 20 years before the onset of symptoms. According to researchers, Porphyromonas Gingivalis could be a cause of Alzheimer's disease. Gum disease is more common, but Alzheimer's disease strikes those who accumulate gingipains and damage the brain quickly enough to develop symptoms during their lifetime, which is considered a universal hypothesis of pathogenesis.

The cortexts report that their COR388 gingipain blockers have entered the brain, have pbaded initial safety tests in humans, and appear to improve those with AD. Larger trials will be launched in search of Porphyromonas Gingivalis in improving cerebrospinal fluid and cognitive abilities, both before and after. The company also plans to test gum disease and create a team in Melbourne to develop a vaccine against Porphyromonas Gingivalis.