Saturday January 19, 2019

A Landmark Study Links Herpes 6 and 7 with Alzheimer’s Disease

The findings also showed multiple points of overlap between virus-host interactions and genes associated with Alzheimer's risk

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For the study, published in the journal Nature, the team engineered a hydrogel that can swell those lymphatic vessels.
For the study, published in the journal Nature, the team engineered a hydrogel that can swell those lymphatic vessels. (IANS)

Scientists have found up to two times higher level of human herpes virus among people with Alzheimer’s disease, suggesting the potential role of the viruses in the development of the progressive brain disorder.

Herpes virus causes contagious sores, most often around the mouth or on the genitals.

The study found unusually increased level of human herpesvirus named human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7 ) in the brains of the people with Alzheimer’s than those without the disorder.

“The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence,” said Richard J. Hodes, Director from the US National Institutes of Health.

“Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defense and innate immune function in the pathophysiology of Alzheimer’s,” said Joel Dudley from the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai.

alzheimers
Patient of Alzheimer’s. Pixabay

The findings also showed multiple points of overlap between virus-host interactions and genes associated with Alzheimer’s risk. Multiple viruses impact the biology of Alzheimer’s disease across domains such as DNA, RNA and proteins.

“If it becomes evident that specific viral species directly contribute to an individual’s risk of developing Alzheimer’s or their rate of progression once diagnosed, then this would offer a new conceptual framework for understanding the emergence and evolution of Alzheimer’s at individual, as well as population, levels,” Dudley explained.

In the study, published in the journal Neuron, the team initially performed RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer’s to quantify which genes were present in the brain, and whether any were associated with the onset and progression of Alzheimer’s.

Also Read: Parkinson’s Identified Gene to Combat Alzheimer’s

Using different computational approaches, the team uncovered a complex network of unexpected associations, linking specific viruses with different aspects of Alzheimer’s biology.

They examined the influence of each virus on specific genes and proteins in brain cells, and identified associations between specific viruses and amyloid plaques, neurofibrillary tangles, and clinical dementia severity.

Further, they incorporated 800, RNA sequencing samples and observed a persistent increase of HHV-6A and HHV-7 in samples from individuals with Alzheimer’s. (IANS)

Next Story

Poor Sleep May Signal The Risk of Alzheimer’s in Elderly

For the study, the team studied 119 people aged 60 or older among which almost 80 per cent were cognitively normal and the remainder were very mildly impaired

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Poor sleep can predict Alzheimer's Risk in elderly. Pixabay

Poor sleep quality may signal the risk of Alzheimer’s disease in older adults, a study suggests.

People with Alzheimer’s tend to wake up tired and their nights become even less refreshing as memory loss and other symptoms worsen.

However, the reason was not fully understood.

The study, led by the Washington University in St. Louis found that older adults who sleep poorly or have less slow-wave sleep — deep sleep needed to consolidate memories and wake up feeling refreshed — have higher levels of tau — a toxic brain protein.

Tau has also been linked to brain damage and cognitive decline.

“Measuring how people sleep may be a non-invasive way to screen for Alzheimer’s disease before or just as people begin to develop problems with memory and thinking,” said lead author Brendan Lucey, Assistant Professor from the varsity.

"The question for us now is not how to eliminate cholesterol from the brain, but about how to control cholesterol's role in Alzheimer's disease through the regulation of its interaction with amyloid-beta," Vendruscolo said.
In Alzheimer’s disease, patients start losing memory, Pixabay

Moreover, the findings, published in the journal Science Translational Medicine, showed that it was not the total amount of sleep that was linked to tau, but the slow-wave sleep, which reflects quality of sleep.

The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep.

“What’s interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired,” Lucey added.

Also Read- Tesla To Retire Lowest-Range Versions of its Model S, X Vehicles

For the study, the team studied 119 people aged 60 or older among which almost 80 per cent were cognitively normal and the remainder were very mildly impaired.

Up to two decades before Alzheimer’s symptoms of memory loss and confusion appear, amyloid beta protein begins to collect into plaques in the brain. Tangles of tau appear later, followed by decline of key brain areas. Only then do people start showing unmistakable signs of cognitive decline.

The challenge is finding people on track to develop Alzheimer’s before such brain changes undermine their ability to think clearly. For that, sleep may be a handy marker, the researchers said. (IANS)