Restoring memory function in Alzheimers disease may now be possible

Henrietta Brewer
January 26, 2019

The findings are published in the latest edition of the journal Science Advances.

Saliva samples from 10 patients with suspected Alzheimer's all proved positive for the P. gingivalis gene. In the paper, an worldwide team of researchers led by Cortexyme co-founders Stephen Dominy, M.D. and Casey Lynch detail the role of a common bacterium, Porphyromonas gingivalis (Pg), in driving Alzheimer's disease pathology, and demonstrate the potential for small molecule inhibitors to block the pathogen.

"The findings of this study offer evidence that P. gingivalis and gingipains in the brain play a central role in the pathogenesis [development] of AD [Alzheimer's disease], providing a new conceptual framework for disease treatment", the study authors write.

Dr Stephen Dominy, one of the study authors and co-founder of the USA company Cortexyme, which developed COR388, said: "Infectious agents have been implicated in the development and progression of Alzheimer's disease before, but the evidence of causation hasn't been convincing".

There have been previous suggestions that it may play a role in Alzheimer's, but the latest study by a US-led worldwide team of scientists appears to put the link beyond question.

Alzheimer's Society highlights the difficulty of accessing NHS Continuing Healthcare (NHS CHC) for people with dementia.

"Not enough people are asking what is upstream of the plaques ... and [brain] inflammation", said Lynch, who has a background in Alzheimer's research and was frustrated by the string of failed therapies for the disease.

Casey Lynch, Cortexyme's co-founder said, 'Despite significant funding and the best efforts of academic, industry, and advocacy communities, clinical progress against Alzheimer's has been frustratingly slow.

Alzheimer's disease is the most common form of dementia, which is characterized by memory loss that gets worse over time. Clumps of a brain protein known as amyloid plaques are a hallmark sign of the disease. So far, there is no cure for the disease. If the findings are shown to be correct, this could offer one reason for why 5.7 million Americans are now living with Alzheimer's disease: a figure set to rise to 14 million by 2050.

It is calling on people to back the campaign, and ensure the government turns its attentions to an issue affecting scores of the 850,000 people living with dementia, and their families.

Previous research observed that Alzheimer's disease patients with the oral infection showed cognitive decline over a six-month period when compared with another group of Alzheimer's disease patients without the infection.

When the team examined the brains and cerebrospinal fluid of Alzheimer's patients, they found DNA from the bacterium.

But the study notes that the bacteria also exist in low levels in 25% of healthy people who did not have any oral disease. "But the evidence of causation hasn't been convincing". With a series of experiments, the researchers showed that one compound, COR388, was able to reduce the bacterial load of a Pg brain infection in mice.

In people with Alzheimer's, tau tangles tend to populate parts of the brain important for memory, such as the hippocampus, before spreading to other areas. The study also finds that in mice, the bacteria trigger brain changes typical of the disease.

The research, a five-year-long study with more than 150 patients in clinical trials, has successfully identified the blood brain barrier as the root of the disease, which affects an estimated 5.7 million Americans. "We will have to see the outcome of this ongoing trial before we know more about its potential as a treatment for Alzheimer's".

The team detected the organism's toxic proteases, or gingipains, in the neurons of patients with Alzheimer's disease.

There is now no test doctors can use to conclusively determine whether someone will get Alzheimer's disease and there are a lot of unknowns about its cause.

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