Dementia is a condition associated with an ongoing decline of brain functioning.According to the NHS, signs and symptoms include memory loss, thinking speed, mental sharpness and quickness and difficulties in carrying out daily activities.New research has found eating at the same time every day could help combat neurodegenerative diseases.Huntington’s Disease is another form of dementia which damages certain nerve cells in the brain, and a new study published in the journal ENeuro found a way to improve quality of life for patients diagnosed with the condition.The study, carried out by researchers from The University of California, LA, found regular meals improved brain power and sleep quality in mice with Huntington’s disease – and they believe it will also apply to humans.As part of the research, one group of mice were only given food during a six-hour period then they were most active.The rest were free to eat whenever they liked.Results revealed the mice who were given regular meal plans to have improved gene expression in the striatum and better cardiovascular health.Study author Professor Christopher Colwell said: “After three months of treatment, when mice reached the early disease stage, they showed improvements in their locomotor activity rhythm and sleep awakening time.“Furthermore, we found improved heart rate variability, suggesting their nervous system dysfunction was improved.“Importantly, treated mice exhibited improved motto performance compared to untreated controls.“The data suggests feeding schedules could play a role in the treatment of dementia and could lead to the development of new treatment options for neurodegenerative disorders.”Having or knowing someone with the condition can be devastating, but there are things in place to make life a little easier.
A DRUG to treat Alzheimer’s could be just five years away after a major breakthrough
Scientists found that destroying specific immune cells reduced the formation of a toxic protein which leads to the disease.
This fresh understanding of the way Alzheimer’s works at a molecular level could finally lead to therapies that treat the underlying causes of the devastating illness.
Experts are trying to develop a “disease-modifying” dementia therapy by 2025.
But Professor Michael Heneka, who led the research at the University of Bonn, Germany, said a drug to stop the disease progressing could come sooner.
Amyloid beta is the rogue protein at the heart of the brain-wasting condition.
Almost all previous trials have targeted the clumps of the protein that build up in sufferers damaging their memories.
The research suggests they are fuelled by inflammation which causes the specific immune cells, called microglia, to release specks of a protein called ASC – which stick to the proteins and cause the clumps to develop.
Analysis shows that Alzheimer’s disease is more feared than cancer in those aged over 45.
Tests on cells grown in a laboratory showed that an antibody blocking ASC from binding to amyloid stopped it from forming into clumps, suggesting progression of the illness can be halted.
The specks have also been seen in scans of brains of those who have died from the disease.
Dr Sara Imarisio, of Alzheimer’s Research UK, said: “Researchers are building a picture of the precise interplay between the immune system and the brain, and this new study adds an important piece to this puzzle.
“By using a sophisticated combination of experiments, these researchers have examined the molecular players linking the immune system and the build-up of amyloid protein from all angles. Research like this is crucial for identifying new avenues to explore in the hunt for new treatments that can slow or halt damaging changes in the brain.”
“Drugs that act against the immune system have real potential to limit damage in Alzheimer’s.”
Alzheimer’s, the most common form of dementia, usually starts with forgetfulness and can progress to complete loss of memory causing the greatest distress to families.
Research shows it doubles in prevalence every five years above the age of 65.
But if onset could be delayed by five years, dementia prevalence would be halved.
The breakthrough, published in the journal Nature, comes as researchers at the University of Manchester, supported by Alzheimer’s Research UK, work on drugs designed to target the molecular machinery inside the brain which, if successful, could pave the way for “life-changing treatments” for dementia, including Alzheimer’s.
There are around a dozen antiamyloid drugs currently in late stage trials but, until now, hope has rested on an experimental drug called aducanumab, a monthly antibody infusion that destroys the build up of plaques.
Test results are due to be published by US drug-maker Biogen in 2019.
Nick Fox, Professor of Neurology at the Institute of Neurology, University College London, said: “For late onset disease, slowing onset for a few years is an effective cure because something else may carry you away. We already have evidence we are seeing effects on brain pathology – will that translate into meaningful clinical benefit in a big trial by 2025? Yes, I think so.”
Professor John Hardy, of the Institute of Neurology at UCL, said: “I am optimistic of finding a disease modifying treatment by 2025. Disease modifying, yes.”
There are now 850,000 people living with dementia in the UK, 500,000 of them with Alzheimer’s, but that number is expected to rocket to a million by 2025.