A sleep disorder that causes repeated shallow or paused breathing may be associated with changes in brain structure that are also seen in the early stages of dementia.
Obstructive sleep apnoea (OSA), common among elderly, is a condition where the walls of the throat relax and narrow during sleep, stopping breathing, and is known to reduce levels of oxygen in the blood. It has also been linked with heart diseases, strokes and cancer.
The new study suggested that the drop in oxygen may be linked to a shrinking of the brain’s temporal lobes and a corresponding decline in memory.
“Between 30 and 50 per cent of the risk for dementia is due to modifiable factors, such as depression, high blood pressure, obesity and smoking. In recent years, researchers have recognized that various sleep disturbances are also risk factors for dementia,” said lead author, Sharon Naismith, from the University of Sydney, Australia.
“We wanted to look specifically at obstructive sleep apnoea and its effects on the brain and cognitive abilities,” Naismith added.
In the study, published in European Respiratory Journal, the researchers analysed data from nearly 100 participants aged between 51 and 88 years, who had visited doctors with concerns over their memory or mood but had no OSA diagnosis.
The results showed that patients who had low levels of oxygen in their blood while they were sleeping tended to have reduced thickness in the left and right temporal lobes of the brain — regions known to be important in memory and affected dementia.
Further, the team found that this alteration in the brain was linked with participant’s poorer ability to learn new information.
“There is no cure for dementia so early intervention is the key. On the other hand, we do have an effective treatment for OSA. This research shows that diagnosing and treating OSA could be an opportunity to prevent cognitive decline before it’s too late,” Naismith added. (IANS)
Eliminating dead-but-toxic cells occurring naturally in the brains of mice designed to mimic Alzheimer’s slowed neuron damage and memory loss associated with the disease, according to a study published Wednesday that could open a new front in the fight against dementia.The accumulation in the body of “zombie cells” that can no longer divide but still cause harm to other healthy cells, a process called senescence, is common to all mammals.
Scientists have long known that these dead-beat cells gather in regions of the brain linked to old age diseases ranging from osteoarthritis and atherosclerosis to Parkinson’s and dementia.
Prior research had also shown that the elimination of senescent cells in ageing mice extended their healthy lifespan.
But the new results, published in Nature, are the first to demonstrate a cause-and-effect link with a specific disease, Alzheimer’s, the scientists said.
But any treatments that might emerge from the research are many years down the road, they cautioned.
In experiments, a team led by Tyler Bussian of the Mayo Clinic in Rochester, Minnesota used mice genetically modified to produce the destructive, cobweb-like tangles of tau protein that form in the neurons of Alzheimer’s patients.
The mice were also programmed to allow for the elimination of “zombie” cells in the same region.
“When senescent cells were removed, we found that the diseased animals retained the ability to form memories, and eliminated signs of inflammation,” said senior author Darren Baker, also from the Mayo Clinic.
The mice likewise failed to develop Alzheimer’s signature protein “tangles”, and retained normal brain mass.
Keeping zombies at bay
A closer look revealed that the “zombies” belonged to a class of cells in the brain and spinal cord, called glia, that provide crucial support and insulation to neurons.
“Preventing the build-up of senescent glia can block the cognitive decline and neuro-degeneration normally experienced by these mice,” Jay Penney and Li-Huei Tsai, both from MIT, wrote in a comment, also in Nature.
Bussian and his team duplicated the results with pharmaceuticals, suggesting that drugs could one day slow or block the emergence of Alzheimer’s by keeping these zombie cells at bay.
“There hasn’t been a new dementia drug in 15 years, so it’s exciting to see the results of this promising study in mice,” said James Pickett, head of research at Alzheimer’s Society in London.
For Lawrence Rajendran, deputy director of the Dementia Research Institute at King’s College London, the findings “open up new vistas for both diagnosis and therapy for neurodegenerative diseases, including Alzheimer’s.”
Up to now, dementia research has been mostly focused on the diseased neurons rather than their neighboring cells.
“It is increasingly becoming clear that other brains cells play a defining role,” Rajendran added.
Several barriers remain before the breakthrough can be translated into a “safe, effective treatment in people,” Pickett and other said.
The elderly often have lots of harmless brain cells that look like the dangerous senescent cells a drug would target, so the molecule would have to be good at telling the two apart.