Posts tagged dementia
Articles and news from the latest research reports.
In Alzheimer’s Disease, Maintaining Connection and ‘Saving Face’
I’ve decided that all older men with gray beards must look alike, because each week I am mistaken for someone else. But, if I were to shave my beard - which I have worn for over 40 years - I believe that my friends and colleagues would fail to recognize me. I would be a different person to them because of this small, physical change.
If such a small change affects the way people see me, then the larger mental changes that Alzheimer’s patients experience must truly and deeply change the way their loved ones see them. Dr. Daniel Potts, a neurologist at the University of Alabama, has begun studying the concept of “saving face” and preserving the “person” in people with dementia.
Dr. Potts’ father, Lester Potts, became an acclaimed watercolor artist after his Alzheimer’s diagnosis. He had lost his verbal abilities but could express his feelings through his art. This bolstered his retention of self-worth and dignity. His paintbrush let him bypass the part of his brain that Alzheimer’s blocked, and communicate in a new way.
But before we find out more about art and Alzheimer’s patients, let’s go back to the “face” part of saving face for just a moment.
(Source: The Atlantic)
Re-learning words lost to dementia
A simple word-training program has been found to restore key words in people with a type of dementia that attacks language and our memory for words.
This ability to relearn vocabulary indicates that even in brains affected by dementia, some recovery of function is possible.
The study, led by Ms Sharon Savage at NeuRA (Neuroscience Research Australia), utilised a simple computer training-program that paired images of household objects such as food, appliances, utensils, tools and clothing, with their names.
“People with this type of dementia lose semantic memory, the memory system we use to store and remember words and their meanings,” says Ms Savage.
“Even the simplest words around the house can be difficult to recall. For example, a person with this type of dementia usually knows what a kettle does, but they may not know what to call it and may not recognize the word ‘kettle’ when they hear it,” she says.
Ms Savage found that after just 3 weeks of training for 30–60 min each day, patients’ ability to recall the name of the items improved, even for patients with more advanced forms of the dementia.
“Semantic dementia is a younger-onset dementia and because sufferers lose everyday words life can be very frustrating for them and their families. By relearning some of these everyday words, day to day conversations around the house may become less frustrating, improving patient well-being,” Ms Savage concludes.
Smoking ‘rots’ brain, says King’s College study
Smoking “rots” the brain by damaging memory, learning and reasoning, according to researchers at King’s College London. A study of 8,800 people over 50 showed high blood pressure and being overweight also seemed to affect the brain, but to a lesser extent.
Scientists involved said people needed to be aware that lifestyles could damage the mind as well as the body. Their study was published in the journal Age and Ageing.
Researchers at King’s were investigating links between the likelihood of a heart attack or stroke and the state of the brain. Data about the health and lifestyle of a group of over-50s was collected and brain tests, such as making participants learn new words or name as many animals as they could in a minute, were also performed.
They were all tested again after four and then eight years. The results showed that the overall risk of a heart attack or stroke was “significantly associated with cognitive decline” with those at the highest risk showing the greatest decline.
It also said there was a “consistent association” between smoking and lower scores in the tests. One of the researchers, Dr Alex Dregan, said: “Cognitive decline becomes more common with ageing and for an increasing number of people interferes with daily functioning and well-being.
"We have identified a number of risk factors which could be associated with accelerated cognitive decline, all of which, could be modifiable." He added: "We need to make people aware of the need to do some lifestyle changes because of the risk of cognitive decline."
The researchers do not know how such a decline could affect people going about their daily life. They are also unsure whether the early drop in brain function could lead to conditions such as dementia.
(Image: Alamy)
Pressure switch inside the head
An increase in cerebral pressure may cause dementia and could destroy the brain. Companies have been seeking to find monitoring sensors that can be implanted into the brain, and read from outside the body. A tiny sensor may provide the help needed.
To this day it remains a mystery why the cerebral pressure in certain people suddenly increases. The consequences, however, are better understood: The blood circulation is disrupted and after a while parts of the brain may die off, similar to what occurs in a stroke. This is how dementia takes its insidious path. Experts estimate that up to ten percent of all cases of dementia in Europe can be attributed to rising blood pressure in the brain. Still, making the diagnosis is tough. People with a heightened susceptibility to a rise in intracranial pressure must be treated with intensive medical care today. A probe is inserted that goes from the outside through the skullcap to the brain. The cable keeps the patient connected to the measuring apparatus. Since cerebral pressure fluctuates, it takes extensive measurements in order to reach a definitive diagnosis of this disease. Patients therefore have to stay in hospital typically for several days, and sometimes even weeks.
New Dementia Diagnostic Exams and Gene Findings Bode Well for Treatment
The number of people affected by dementias continues to climb as baby boomers age, increasing the urgency to identify ways to prevent, diagnose and treat these neurodegenerative brain disorders.
Today it is possible to diagnose dementias more accurately than ever before, thanks to improvements in behavioral assessment tools, imaging techniques, gene testing and data collection and analysis, according to Bruce L. Miller, MD, a behavioral neurologist and professor of neurology at UCSF.
Miller, who came to UCSF in 1998 and directs the UCSF Memory and Aging Center, described recent advances during the lecture he gave at UCSF Mission Bay on Oct. 15 as part of receiving the Academic Senate’s 12th Annual Faculty Research Lectureship in Clinical Science.
The ability to diagnose different types of dementias accurately and to distinguish among the biological factors that cause them will become increasingly important as treatments become more promising and better targeted, Miller said.
Despite continued improvements in the tools available to physicians for diagnosing dementias, a common neurodegenerative disease known as frontotemporal dementia (FTD) remains understudied and is very often misdiagnosed, Miller said. For reasons that are in part historical, FTD still is thought of as a rare disease, a misconception that greatly contributes to its being underdiagnosed, he said. While Alzheimer’s disease is the most common dementia overall, among the population aged 65 and younger, FTD is just as common, according to Miller.
Clue to Alzheimer’s cause found in brain samples
Researchers at Washington University School of Medicine in St. Louis have found a key difference in the brains of people with Alzheimer’s disease and those who are cognitively normal but still have brain plaques that characterize this type of dementia.
“There is a very interesting group of people whose thinking and memory are normal, even late in life, yet their brains are full of amyloid beta plaques that appear to be identical to what’s seen in Alzheimer’s disease,” says David L. Brody, MD, PhD, associate professor of neurology. “How this can occur is a tantalizing clinical question. It makes it clear that we don’t understand exactly what causes dementia.”
Hard plaques made of a protein called amyloid beta are always present in the brain of a person diagnosed with Alzheimer’s disease, according to Brody. But the simple presence of plaques does not always result in impaired thinking and memory. In other words, the plaques are necessary – but not sufficient – to cause Alzheimer’s dementia.
The new study, available online in Annals of Neurology, still implicates amyloid beta in causing Alzheimer’s dementia, but not necessarily in the form of plaques. Instead, smaller molecules of amyloid beta dissolved in the brain fluid appear more closely correlated with whether a person develops symptoms of dementia. Called amyloid beta “oligomers,” they contain more than a single molecule of amyloid beta but not so many that they form a plaque.
Oligomers floating in brain fluid have long been suspected to have a role in Alzheimer’s disease. But they are difficult to measure. Most methods only detect their presence or absence, or very large quantities. Brody and his colleagues developed a sensitive method to count even small numbers of oligomers in brain fluid and used it to compare amounts in their samples.
The researchers examined samples of brain tissue and fluid from 33 deceased elderly subjects (ages 74 to 107). Ten subjects were normal – no plaques and no dementia. Fourteen had plaques, but no dementia. And nine had a diagnosis of Alzheimer’s disease – both plaques and dementia.
They found that cognitively normal patients with plaques and Alzheimer’s patients both had the same amount of plaque, but the Alzheimer’s patients had much higher oligomer levels.
But even oligomer levels did not completely distinguish the two groups. For example, some people with plaques but without dementia still had oligomers, even in similar quantity to some patients with Alzheimer’s disease. Where the two groups differed completely, according to Brody and his colleagues, was the ratio of oligomers to plaques. They measured more oligomers per plaque in patients with dementia, and fewer oligomers per plaque in the samples from cognitively normal people.
In people with plaques but no dementia, Brody speculates that the plaques could serve as a buffer, binding with free oligomers and keeping them tied down. And in dementia, perhaps the plaques have exceeded their capacity to capture the oligomers, leaving them free to float in the brain’s fluid, where they can damage or interfere with neurons.
Brody cautions that, due to the difficulty in getting samples, oligomer levels have never been measured in living people. Therefore, it’s possible these floating clumps of amyloid beta only form after death. Even so, he says, there is still a clear difference between the two groups.
“The plaques and oligomers appear to be in some kind of equilibrium,” Brody says. “What happens to shift the relationship between the oligomers and plaques? Like much Alzheimer’s research, this study raises more questions than it answers. But it’s an important next piece of the puzzle.”
(Source: news.wustl.edu)
Doctors took an hour to realise Sarah Merriman had Down’s syndrome after her birth in January 1992. By then, her father, Andy, had phoned friends and family to tell them his wife, Alison, had given birth to a healthy baby. His happy news was dashed. “It was a real shock,” Andy recalls. “From the start, we were warned about the difficulties and troubles that lay ahead for Sarah. Then she was diagnosed as having a hole in her heart. The worry, for the first years of her life, was constant.”
Sarah’s heart healed. She did well at her school in Haringey, north London, and went on to pass the equivalent of four GCSEs. Today, she is studying catering and lives with other students near her college in Somerset. “Sarah is independent and copes with life in a way we could never have imagined just after she was born,” says Andy.
It is a reassuring story, although one major worry still besets the Merriman family: Sarah’s long-term future and her susceptibility to Alzheimer’s disease, a form of dementia that leads to complete loss of memory, speech and awareness and which is closely linked to Down’s syndrome. Among members of the general population, the risk of getting Alzheimer’s before the age of 65 is less than 5%. For a person with Down’s syndrome the figure is 50%.
Could Down’s syndrome point the way to preventing Alzheimer’s disease?
The Dementia and Music Project - Chloe Meineck
This project is a culmination of two years research highlighting the advantages of listening to familiar music for dementia sufferers. This coupled with the fact that when many people move into a home they feel lost in their unfamiliar surroundings. The music box, which is all hand made, combines an interactive music player, with a memory box of co-designed special objects.
The film is Barbara talking about her life, her most important objects, music, events and her most treasured people.
Gladstone Scientists Identify Biological Mechanism that Plays Key Role in Early-Onset Dementia: Findings explain how protein deficiency contributes to neurodegenerative disease
Using animal models, scientists at the Gladstone Institutes have discovered how a protein deficiency may be linked to frontotemporal dementia (FTD)—a form of early-onset dementia that is similar to Alzheimer’s disease. These results lay the foundation for therapies that one day may benefit those who suffer from this and related diseases that wreak havoc on the brain.
As its name implies, FTD is a fatal disease that destroys cells, or neurons, that comprise the frontal and temporal lobes of the brain—as opposed to Alzheimer’s which mainly affects brain’s memory centers in the hippocampus. Early symptoms of FTD include personality changes, such as increased erratic or compulsive behavior. Patients later experience difficulties speaking and reading, and often suffer from long-term memory loss. FTD is usually diagnosed between the ages of 40 and 65, with death occurring within 2 to 10 years after diagnosis. No drug exists to slow, halt or reverse the progression of FTD.
A new study led by Gladstone Senior Investigator Robert V. Farese, Jr., MD, offers new hope in the fight against this and other related conditions. In the latest issue of the Journal of Clinical Investigation, Dr. Farese and his team show how a protein called progranulin prevents a class of cells called microglia from becoming “hyperactive.” Without adequate progranulin to keep microglia in check, this hyperactivity becomes toxic, causing abnormally prolonged inflammation that destroys neurons over time—and leads to debilitating symptoms.
Dementia: The Self-Portraits of William Utermohlen
About the art work: When he learned in 1995 that he had Alzheimer’s disease, William Utermohlen, an American artist living in London, immediately began work on an ambitious series of self-portraits. The artist pursued this project over an eight-year period, adapting his style to the growing limitations of his perception and motor skills and creating images that powerfully documented his experience of his illness. The resulting body of work serves as a unique artistic, medical, and personal record of one man’s struggle with dementia.
Full Article: The Dementia Plague