High BP in late life may protect against dementia: study

Washington D.C., Jan 12: Disruption in one night's sleep can lead to getting Alzheimer's disease, a recent study has stated.

The interruption in the sound sleep for a single night aggravates the level of tau protein in any young male's body, thus gives rise to the chances of developing the disease.

According to CNN, the report was published on Wednesday in neurology, the medical journal of the American Academy of Neurology.

"Our study focuses on the fact that even in young, healthy individuals, missing one night of sleep increases the level of tau in blood suggesting that over time, such sleep deprivation could possibly have detrimental effects," says study author Dr Jonathan Cedernaes, a neurologist at Uppsala University in Sweden.

As defined by the Alzheimer's Association, tau is the name of a protein that helps in stabilizing the internal structure of the brain's nerve cells. An abnormal build-up of tau protein in the body can end up in causing interior cells to fall apart and eventually developing Alzheimer's.

"When you get more of that deep sleep and you get the REM sleep in the normal amounts, that improves clearance of abnormal proteins which we think is good," said Mayo Clinic neurologist Dr Donn Dexter, not the study author but a fellow of the American Academy of Neurology.

Earlier studies have also shown that getting deprived of sleep can allow higher tau development and accumulation. Thus that poor sleep can hasten the development of cognitive issues.

Researchers caution that the study is small and inconclusive, and acknowledged they were not able to determine what the increased levels might mean.

"This study raises more questions than answers," agreed Dexter on a concluding note, sharing, "What this is telling us is that we have to dig more deeply. Despite something we do for a third of our lives, we know so little about sleep and we're learning every day, particularly when it comes to sleep and dementia."

Apart from the many benefits of doing exercise, new research has now found that exercise can slow down or prevent the development of macular degeneration and may benefit other common causes of vision loss, such as glaucoma and diabetic retinopathy.

The new study from the University of Virginia School of Medicine found that exercise reduced the harmful overgrowth of blood vessels in the eyes of lab mice by up to 45 per cent. This tangle of blood vessels is a key contributor to macular degeneration and several other eye diseases.

The study represents the first experimental evidence showing that exercise can reduce the severity of macular degeneration, a leading cause of vision loss, the scientists report. Ten million Americans are estimated to have the condition.

"There has long been a question about whether maintaining a healthy lifestyle can delay or prevent the development of macular degeneration. The way that question has historically been answered has been by taking surveys of people, asking them what they are eating and how much exercise they are performing," said researcher Bradley Gelfand, PhD, of UVA's Center for Advanced Vision Science.

"That is basically the most sophisticated study that has been done. The problem with that is that people are notoriously bad self-reporters ... and that can lead to conclusions that may or not be true. This [study] offers hard evidence from the lab for the very first time," Gelfand added.

Enticingly, the research found that the bar for receiving the benefits from exercise was relatively low - more exercise didn't mean more benefit.

"Mice are kind of like people in that they will do a spectrum of exercise. As long as they had a wheel and ran on it, there was a benefit. The benefit that they obtained is saturated at low levels of exercise," Gelfand said.

An initial test comparing mice that voluntarily exercised versus those that did not found that exercise reduced the blood vessel overgrowth by 45%. A second test, to confirm the findings, found a reduction of 32 per cent.

The scientists aren't certain exactly how exercise is preventing the blood vessel overgrowth. There could be a variety of factors at play, they say, including increased blood flow to the eyes.

Gelfand, of UVA's Department of Ophthalmology and Department of Biomedical Engineering, noted that the onset of vision loss is often associated with a decrease in exercise.

"It is fairly well known that as people's eyes and vision deteriorate, their tendency to engage in physical activity also goes down. It can be a challenging thing to study with older people. ... How much of that is one causing the other?" he said.
The researchers already have submitted grant proposals in hopes of obtaining funding to pursue their findings further.

"The next step is to look at how and why this happens, and to see if we can develop a pill or method that will give you the benefits of exercise without having to exercise," Gelfand said.

He explained, "We're talking about a fairly elderly population [of people with macular degeneration], many of whom may not be capable of conducting the type of exercise regimen that may be required to see some kind of benefit." (He urged people to consult their doctors before beginning any aggressive exercise program.)
Gelfand, a self-described couch potato, disclosed a secret motivation for the research: "One reason I wanted to do this study was sort of selfish. I was hoping to find some reason not to exercise," he joked. "It turned out exercise really is good for you."

Washington DC, Apr 17: In recent research, scientists have linked the emotional, social and psychiatric problems in children and adolescents with higher levels of genetic vulnerability for adult depression. The study implies that the genetics passed from parents may be linked with psychiatric problems in children and adolescents and may also leading to depression in adults.

University of Queensland scientists made the finding while analysing the genetic data of more than 42,000 children and adolescents from seven cohorts across Finland, the Netherlands, Norway, Sweden and the UK.

Professor Christel Middeldorp said that researchers have also found a link with a higher genetic vulnerability for insomnia, neuroticism and body mass index.

"By contrast, study participants with higher genetic scores for educational attainment and emotional well-being were found to have reduced childhood problems," Professor Middeldorp said.

"We calculated a person's level of genetic vulnerability by adding up the number of risk genes they had for a specific disorder or trait and then made adjustments based on the level of importance of each gene We found the relationship was mostly similar across ages," Middeldorp added.

The results indicate there are shared genetic factors that affect a range of psychiatric and related traits across a person's lifespan.

Middeldorp said that around 50 per cent of children and adolescents with psychiatric problems, such as attention deficit hyperactivity disorder (ADHD), continue to experience mental disorders as adults, and are at risk of disengaging with their school community among other social and emotional problems.

"Our findings are important as they suggest this continuity between childhood and adult traits is partly explained by genetic risk," the Professor said.

"Individuals at risk of being affected should be the focus of attention and targeted treatment," Middeldorp continued.

"Although the genetic vulnerability is not accurate enough at this stage to make individual predictions about how a person's symptoms will develop over time, it may become so in the future, in combination with other risk factors. And, this may support precision medicine by providing targeted treatments to children at the highest risk of persistent emotional and social problems," Middeldorp added.