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- The bacterium in periodontitis seems to be the culprit.
- The accumulations of amyloid and tau reported may be an answer, not a cause.
- A convincing research is a real reason to be optimistic.
Dementia is now the fifth leading cause of death in the world, and 70% of it is due to Alzheimer's disease. Until now, experts have been puzzled by its causes and powerless to slow down or reverse the cruel progress of this disease. Alzheimer's keeps his victims away from reality as their families look at him, heartbroken, until death carries the coup de grace. This could be about to change, however, thanks to new research that is discovering that the cause of Alzheimer's is actually a bacteria, P gingivalis, in gum disease.
Has the role of protein deposition in patients' brains been misunderstood?
(NIH Image Gallery)
Brain with plaque buildup in blue
It has long been known that the brain of Alzheimer's disease sufferers contains unusually high amounts of amyloid protein and tau protein. This has naturally led to think that these proteins are at the origin of the disease. However, it turns out that some older people with exceptional memories have a significant amount of amyloid protein and tau protein in their brains. This has challenged their causal role in the disease and is leading scientists to investigate the possibility that proteins appear as reply to the real culprit.
Gum disease in mice
(NIH Image Gallery)
P. gingivalis
2009 research identified a bacterium causing gum disease IgG P gingivalis, as a common disease of Alzheimer's suffers and is frequently present in the brain. However, it was unclear whether patients' periodontitis was related to the disease or was simply a disease that the patients had contracted after its onset.
A number of research teams have P gingivalis experiments and revealed that its presence worsens the symptoms of Alzheimer's disease – including accumulation of amyloid – in mice reproduced for the disease, and actually causes the disease. Alzheimer's in healthy mice.
An early index
(Arigo Biolaboratories)
A few years ago, Robert Moir of Mbadachusetts General Hospital began to examine the behavior of a particular amino acid sequence in beta-amyloids. It exists in 70% of vertebrates, as well as in other animals, which intrigues Moir, who told the New Scientist: "It is a very old peptide that does something important. " He discovered that the protein was a killer of bacterial microbes. This suggests that familiar accumulations could defend the brain against invading bacteria.
The smoking gun
(Dominy et al)
The new study reveals that toxic enzymes, gingipaine, that allow P gingivalis Feeding human flesh was found in 96% of the examined tissues on 54 Alzheimer's sufferers. In addition, when they examined the DNA of three Alzheimer's brains, they found that P gingivalis at the shopping mall. Researcher Sim Singhrao of Central Lancashire University, not involved in the study, explains to New Scientist: "This is the first report showing that DNA from P. gingivalis in the human brain and badociated Gingipains co-locate with plaques. "
As further confirmation, there were more bacteria and its gingipaines – and amyloid and tau accumulation – in patients with more advanced dementia.
The study also revealed that gingipaines were transforming tau proteins into proteins so that they start killing neurons. The result? Dementia.
What does it mean
All in all, this could ultimately be the breakthrough expected by Alzheimer's scientists.
- First of all, the researchers discovered P gingivalis in the cerebrospinal fluid of living patients, suggesting a means of early diagnosis, since Alzheimer's disease can take 10 to 20 years before becoming symptomatic.
- Second, bacteria can be vulnerable to treatment. The pharmaceutical company Cortexine is testing gingipain inhibitors that have resulted in improvement in patients with Alzheimer's disease. More important lawsuits are imminent.
- Third, another team in Melbourne Australia is working on a vaccine against gum disease and therefore Alzheimer's disease.
The beginning of the end of Alzheimer's?
We had hoped before, but the new research provides a real reason for optimism. The cause of this tragic situation may have finally been identified. As Casey Lynch, of Cortexme, says, "we think it's a universal hypothesis of pathogenesis".
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