Sleep deprivation accelerates Alzheimer's brain damage

Scientists May Have Found a Way to Restore Memory Function in Alzheimer's Patients

Risk Factors involved with the disease and that age is the greatest known risk factor for Alzheimer's, include an individuals risk for developing Alzheimer's increases after the age of 65, having a parent or sibling with the disease increases an individuals risk and 5.7 million people are now living with Alzheimer's.

AD results from both genetic and environmental risk factors, such as aging, which combine to result in epigenetic changes, leading to gene expression changes, but little is known about how that occurs.

Researchers from the institute conducted the study in collaboration with neurologists from the Washington University School of Medicine in St. Louis and the Huntington Medical Research Institutes in Pasadena. They tested the tissue samples for the presence of 2 protein fragments produced by P. gingivalis bacteria, called gingipains to see if people with Alzheimer's disease had more gingipains in their brain tissue.

An incredible discovery by medical researchers could change the treatment of Alzheimer's disease as we know it, now that a simple blood test could identify the condition over a decade before it sets in. Montagne said. "If we find a cure, if we find a way to seal the blood barrier, we may be able to help cure other diseases".

"We collect blood, spinal fluid and urine to try and look for ... what people like to call biomarkers of Alzheimer's disease", said Michael Harrington, a director of neuroscience and research at HMRI.

Some brain samples from people without Alzheimer's also had P. gingivalis and protein accumulations, but at lower levels. In 2017, it was shown that deliberate infection gum-disease bacteria caused amyloid pathology and cognitive decline in a transgenic mouse model. Recent research at WUSM has shown that tau is high in older people who sleep poorly. Giving mice a gingipain-inhibiting substance by mouth twice a day treated the brain infection and was better at reducing bacterial load than the antibiotic moxifloxacin (a recommended treatment for people with gingivitis). When the mice were disturbed during times they were typically asleep or resting, their tau levels doubled. According to Brendan Lucey, MD the same effect was seen in humans; after as sleepless night tau levels were found to increase by 50%.

The results suggest that tau is typically released in brains during waking hours by thinking and doing things and the release is then slowed during sleep, allowing tau to be cleared away, the researchers said.

Most notable is whether or not the bacteria promotes Alzheimer's or if it's simply a byproduct of the brain disease. That tangled tau eventually spreads to other portions of the brain, clouding a person's ability to think.

The mouse studies found that blocking gingipains effectively protected the hippocampus, a part of the brain vital to memory, from P. gingivalis infection. After four weeks, the mice that were repeatedly kept up had more widespread tau tangles. The new blood test detects a type of protein known as "Neurofilament light polypeptide (NLP)" that normally resides inside neurons, and makes part of their internal skeleton.

The study is still ongoing, but 243 were already found to have increasing levels of the protein. It's worth noting that not all people with Alzheimer's had P. gingivalis in their cerebrospinal fluid - and there was no comparison group without Alzheimer's.

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