To prevent it, it is important to remove the stigma attached to it
It was found in a recent survey
Reducing stigma attributed to Alzheimer’s disease is vital for prevention research, a new study suggests, adding that the stigma associated with the disease may be an obstacle for individuals to seek information about their risk of developing it.
The survey focused on what beliefs, attitudes and expectations are most often associated with the disease. “We found that concerns about discrimination and overly harsh judgments about the severity of symptoms were most prevalent,” said co-author of the study, Shana Stites from the University of Pennsylvania. “By understanding what the biggest concerns are about the disease, we can help develop programmes and policies to reduce the stigma about Alzheimer’s disease,” Stites added.
For the study, published in the journal Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association, a random sample of 317 adults was asked to react to a fictional description of a person with mild stage Alzheimer’s disease dementia.
The study asked respondents to read a vignette and then complete the survey. Three different assessments were presented for the fictional person’s condition. Respondents were told the person’s condition would worsen, improve or remain unchanged. Over half of the respondents (55 percent) expected the person with mild cognitive impairment or dementia due to Alzheimer’s to be discriminated against by employers and to be excluded from medical decision-making.
Almost half expected the person’s health insurance would be limited due to data in the medical record (47 percent), a brain imaging result (46 percent) or genetic test result (45 percent). Those numbers increased when the participants were informed that the condition of the person with Alzheimer’s would worsen over time, the researcher said. 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.