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Sleep Deprivation Quickens Spread Of Tau

Sleep Deprivation Quickens Spread Of Tau

"We will have to see the outcome of this ongoing trial before we know more about its potential as a treatment for Alzheimer's".

Research published Wednesday in the journal Brain shows a possible solution by focusing on the emerging field of neurobiology called epigenetics. In fact, the samples show a spectrum of all these proteins, with the Alzheimer's samples invariably on the high side and the controls invariably on the low.

Findings were revealed in a study from the Washington University School of Medicine which suggests real life factors such as sleep may affect how fast the disease spreads. In the paper, an global 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 research team, which is coordinated by pharma startup Cortexyme that was co-founded by first author Stephen Dominy, isn't claiming to have discovered definitive evidence of Alzheimer's causation. Yet.

Tau exists normally in the brain but becomes toxic in Alzheimer's.

James Pickett, head of research at the UK's Alzheimer's Society pointed out that the study's participants had a faulty gene "which causes an inherited form of the disease".

One drug, given to mice in food, effectively treated P. gingivalis brain infections and prevented the loss of memory neurons. The team also found the bacteria in the spinal fluid of living people with Alzheimer's, suggesting that this technique may provide a long-sought after method of diagnosing the disease.




They also showed that when genetically modified mice who were predisposed to Alzheimer's were infected with P. gingivalis, the bacterium ended up in their brain and that this was associated with increased levels of amyloid protein.

"That is why we have created highly potent, brain penetrant, anti-gingipain small molecules to target P. gingivalis and gingipians in the brain", he said. Giving some of these to mice reduced their infections, halted amyloid production, lowered brain inflammation and even rescued damaged neurons. The bacteria was found in three brain tissue DNA samples. They did not resist the gingipain blockers.

Writes Science Advances, in recent years, scientists are finding more evidence to support the hypothesis on the infectious nature of Alzheimer's disease.

Their NFL protein levels were measured through a blood test, brain images, and cognitive tests every 2.5 years, over the last seven. This, says Lynch, shows P. gingivalis is a cause of Alzheimer's, not a result.

Although there is still no cure for Alzheimer's disease, the possibility of treating the condition more than a decade before it develops opens a world of new possibilities.

They add: "We also demonstrated [in living animals] that an orally-administered [gingipain] inhibitor is more effective than a high-dose subcutaneous broad spectrum antibiotic in clearing P. gingivalis from the brain".

"In this paper, we have not only identified the epigenetic factors that contribute to the memory loss, we also found ways to temporarily reverse them in an animal model of AD", said senior author Zhen Yan, PhD, a SUNY Distinguished Professor in the Department of Physiology and Biophysics in the Jacobs School of Medicine and Biomedical Sciences at UB.

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