Read news from Honolulu at the Alzheimer’s conference

July 13, 2010

If you couldn’t make it to Honolulu, (darn! me neither!) you can still stay up-to-date with what is happeneing at the International Conference on Alzheimer’s Disease by reading the daily news releases. The web address is www.alz.org/icad.


Scientists study jellyfish for ways to preserve cognition in Alzheimer’s and other dementias

July 13, 2010

A biotech company in Madison, Wisconsin believes a protein from a jellyfish (with the scientific name, Aequorea victoria) can improve cognitive function in people with memory problems, Alzheimer’s disease or other dementias.

Quincy Bioscience representatives are at the annual Alzheimer’s Association International Conference on Alzheimer’s Disease this week in Honolulu, presenting interim data that demonstrates the jellyfish protein improved cognitive testing scores by 14 percent in 60 days compared to placebo in the randomized controlled “Madison Memory Study,” which enrolled adults who had a memory concern. The average age in the study cohort of 35 people was 61 years old.

Why the jellyfish?

Partly because of its simplicity. “If you strip down all of the higher functions of thought from the human brain, you really end up with a very simple nervous system…as simple as the jellyfish,” says the Quincy website. Scientists have been studying the design of the jellyfish to understand how it might protect brain cells. Jellyfish make use of apoaequorin to sequester extra calcium ions, which are thought to be protective against neurodegeneration.

In diseases such as Alzheimer’s and Parkinson’s,  calcium-binding proteins decrease and lead to brain cell death, or neurodegeneration. Scientists believe that by managing calcium levels in the cells, they can slow the aging process and preserve some quality of life.


Understanding what the ‘Preventing Alzheimer’s Disease and Cognitive Decline’ panel said about the state of the science

June 30, 2010
Download the 21-page “Preventing Alzheimer’s Disease and Cognitive Decline”
state-of-the-science conference statement

A call for mainstreaming people with Alzheimer’s; ‘what’s the harm in that?’

June 24, 2010

As soon as a person is diagnosed with Alzhiemer’s, friends often disappear–even quite early on when the person is just a bit forgetful.

“They think it might all be a bit too awkward,” Julian Hughes says of the friends.

“But attitudes must change. Those friends can adjust, let the conversation go with the flow, accept the person with dementia may be living within a few minutes of experience, so you may have to repeat your stories. But what’s the harm in that? If they are enjoying it, then it’s still a meaningful experience.”

Hughes is a British psychiatrist who specializes in aging–his academic interest is the notion of personhood–and recently he spoke throughout Australia, calling for mainstreaming of those with Alzheimer’s and other dementias and for governments to recognize this significant health issue. He also made the point that research funding for Alzheimer’s lags hugely behind other areas, such as cancer. “As the numbers (of diagnosed) rise, funding will need to increase by a factor of six to eight times to keep pace,” Hughes points out.

Dementia is the third-leading cause of death in Australia, behind heart disease and stroke. About 257,000 Australians have dementia today, and that’s expected to rise to more than a million by 2050.

In America, deaths from Alzheimer’s disease are almost equal to those from diabetes, and both rank below heart disease, cancer, respiratory disorders and accidents. But that’s expected to change in the coming years, as Baby Boomers begin hitting age 65. Today, 5.1 million Americans have Alzheimer’s disease; that number will climb to 13.5 million by 2050, says a report from the Alzheimer’s Association, which says the costs of care will inevitably rise, too, from $172 million today to more than $1 trillion by 2050.

Read the story in The Australian.

Read my previous post about the rising cost of Alzheimer’s.


Apple juice found helpful for those with Alzheimer’s disease

June 22, 2010

Behavioral and psychotic symptoms related to dementia seem to improve when people with moderate-to-late stage Alzheimer’s disease regularly drink apple juice.

That’s what researchers from the University of Massachusetts found in a study published in the June 2010 issue of American Journal of Alzheimer’s Disease and Other Dementias.

For their study, the researchers assigned 21 individuals with moderate to severe Alzheimer’s disease to drink a 4-oz glass of apple juice twice a day for one month.

Though caregivers reported reduction in anxiety, agitation and delusion, the individuals with dementia showed no changes in the Dementia Rating Scale.

Previous studies have suggested that apple juice may provide health benefits including reduction of central nervous system oxidative damage, suppression of Alzhiemer’s symptoms, improved cognitive performance and more organized synaptic signaling. Thomas Shea says other researchers have shown similar effects with blueberries. “We have also shown similar effects with purified vitamins and nutriceuticals.” Shea is professor of biological sciences and Director of the Center for Cellular Neurobiology & Neurodegeneration Research at Massachusetts.

Would apple juice be helpful in people with other dementias?

“We saw in mice that apple juice boosted neurotransmitter production, so it might help us all with mood, and the major effect would be seen on those individuals, disease or not, that had behavioral issues,” he says. “However, it is certainly worth a try.”

Shea says he would like to compare apple juice with apple cider in another study because “cider has the potential benefit of being fresher, and less processed.”

Read the article from FoodConsumer.

Read the abstract from the American Journal of Alzheimer’s Disease & Other Dementias.


Finding a link between PTSD and dementia raises the question of why

June 18, 2010

Male military veterans with PTSD were found to have a nearly 2-fold-higher risk of developing dementia, compared to those without post-traumatic stress disorder, an anxiety disorder that is highly prevalent because of combat. Results of a study into this link are published in this month’s Archives of General Psychiatry.

The study involved 181,093 veterans 55 years or older without dementia from 1997 through 2000. Between 2000 and 2007, researchers discovered 17 percent of the men developed dementia, according to the abstract by Dr. Kristine Yaffe and colleagues at the University of California, San Francisco, and San Francisco Veterans Affairs Medical Center. They presented their work last year in Vienna at the International Conference on Alzheimer’s Disease.

“Mechanisms linking these important disorders need to be identified with the hope of finding ways to reduce the increased risk of dementia associated with PTSD,” they write. Some theories: that PTSD contributes to the cause of dementia, that chronic stress plays a role, or that stress damages the hippocampus or cause alterations in neurotransmitter and hormone levels that could precipitate dementia.

Finding a link between PTSD and dementia was not entirely surprising. “We already know that traumatic brain injury and certainly chronic stress increase the risk of cognitive decline and what this paper refers to as ‘accelerated aging,’ which may in turn lead to early dementia. So it makes sense that PTSD would increase the risk for dementia in the long run,” Maria C. Carrillo, a senior director for the Alzheimer’s Association, told Medscape.

Read the Medscape article.

Read the abstract from the Archives of General Psychiatry.


Locating genes for clues to Alzheimer’s risk, cause, diagnosis

June 15, 2010

Neuroscientists have zeroed in on some target genes that may be tied to the development of Alzheimer’s disease, and they’ve shown what abnormalities appear on brain scans of people with these genetic variations.

Both bits of scientific progress are incremental steps toward understanding what causes the disease that afflicts more than 5 millon Americans. The study, lead by researchers in Boston and Cambridge, Mass., England and Wales, appears in this month’s Archives of Neurology.

“The drought of genetic findings in Alzheimer’s disease has lasted a long time,” write scientists based in London and Wales in an editorial accompanying the Archives study. “These findings, and the genome-wide studies that presaged them, mark a new period of optimism for those of us who study the etiologies of complex diseases of the nervous system.”

The study explains the association researchers made between genetic loci that are related to Alzheimer’s disease and neuorimaging measures that are related to disease risk. (These measures include the volume of the hippocampus, amygdala and other brain structures.) They identify B1N1 and CNTN5 as additional specific locations of genetic variants on chromosomes, but say their findings warrant further study.

Just one genetic variant, known as APOE, has been shown to influence Alzheiemer’s disease risk and age at onset, lead authors Drs. Alessandro Biffi and Christopher Anderson write in their background information.

Study participants included 168 people with probable Alzheimer’s, 357 people with mild cognitive impairment, a precursor to Alzheimer’s, and 215 people who were cognitively normal. “Our results indicate that APOE and other previously validated loci for Alzheimer’s disease affect clinical diagnosis of Alzheimer’s disease and neuroimaging measures associated with the disease,” they write.

Will that bring us closer to genetic tests for Alzheimer’s?

Somewhat, John Hardy, of the University College London Institute of Neurology, says in an email, “but I think this genetic determinism argument is oversold, frankly.

“About 5 percent of the population are at high risk. About 30 percent of the population are at a moderate risk, and about 65 percent are at lower risk. These numbers are little changed by the new data. And, this is not really so useful for genetic testing.”

Read the study in the Archives of Neurology.

The National Institute on Aging’s fact sheet on Alzheimer’s disease genetics.


Cases of doggy dementia go undiagnosed

June 9, 2010

Dogs get dementia, too.

It’s called canine cognitive dysfunction.

And it’s especially interesting, from a research point of view, because canine brains more closely resemble human brains than those of laboratory rats. Also, since so so many dogs are members of human families, they are subject to many of the same environmental factors as humans.

Most senior-age dogs with dementia go undiagnosed, according to a recent study in The Veterinary Journal. Veterinary scientists at the University of Sydney studied 1,000 dogs and found 14 perent had dementia. Only about 2 percent had been diagnosed. (Researchers found no appreciative difference among breeds, by the way.)

”Like dementia in humans, canine dementia often ruins the bond between the sufferer and their carer because the dog no longer seems to recognise the owner or may develop annoying habits,” Hannah Salvin, a doctoral student at the university who led the study, told the Sydney Morning Herald.

As with humans, the disease is incurable.

Some treatments are emerging, though, and associate professor Paul McGreevy told the newspaper “their responses could provide us with pivotal information about the potential therapeutic effects in humans.”

Salvin and McGreevy are interested in studying more dogs in the greater Sydney area. Their website, maturedogs.com, provides details.

Symptoms

Pacing, circling, wandering.

Failure to recognise familiar people or pets.

Walking into walls or furniture.

Standing over water bowl, not drinking.

Avoiding being petted or touched.

House soiling.

Read the story in the Sydney Morning Herald.

Read the abstract from The Veterinary Journal.

Learn more about Cognitive Dysfunction Syndrome in dogs, from Pfizer.


Research into cognition explains some age-related memory loss

June 7, 2010

You really can’t teach an old dog new tricks. Well, not if you expect the dog to remember the trick.

Through research into cognitive decline, scientists have demonstrated that “there is a biological reason why people cannot learn new things at an older age, but can retain knowledge learned years before,” says John Morrison, dean of basic sciences and the graduate school of biological sciences at Mount Sinai School of Medicine.

Certain types of specializations on nerve cells called “spines” are depleted as someone ages, causing cognitive decline in the part of the brain mediating the highest levels of learning, he explains in a study published June 2 in the Journal of Neuroscience.

We lose certain spines as we age, but this study explains which ones and how their loss impacts cognition–which may lead scientists to develop new therapies that target age-related cognitive decline.

The research team studied six young adult and nine older rhesus monkeys as they participated in a delayed response test. The monkeys watched as food was baited and hidden. Then a screen was put in front of them so they could no longer see the location of the hidden reward. At the beginning of the test, the screen was raised immediately, and the monkeys found the reward right away. The memory of the monkeys was tested by increasing the time the reward was blocked from view. The aged monkeys performed significantly worse on the tests than young monkeys, especially as the time intervals increased, researchers reported.

They then studied the microscopic changes in the nerve cells within the prefrontal cortex, an area of the brain that mediates high level learning. Nerve cells in this area contain both thin, dynamic spines which are key to learning new things, as well as large, mushroom-shaped spines that likely mediate long-term memories and expertise. The older monkeys lacked the thin spines but retained the larger spines, “indicating that the loss of the thin spines may be responsible for monkeys’ inability to learn and retain information during the test,” says a news release from Mount Sinai.

Read the abstract.

Read the article in Science Daily.


A curious study of Agatha Christie and Alzheimer’s — and how our writings may one day be used for diagnosis

June 4, 2010

The language of people with Alzheimer’s disease includes significantly more indefinite words and repetitions than the language of healthy people of similar age and level of education.

So, an English professor at the University of Toronto, Ian Lancashire, analyzed the writing of British mystery writer Agatha Christie.

Previously, the works of British novelist Iris Murdoch were analyzed for signs of the Alzheimer’s disease that was confirmed after her death. Science Blog reported in 2004 that “while the structure and grammar of Murdoch’s writing remained roughly consistent throughout her career, her vocabulary had dwindled and her language simplified in her very last novel.”

Christie was never diagnosed with Alzheimer’s. She continued to write in her final years, though some people believed she suffered from dementia.

Lancashire says her 73rd book, “Elephants Can Remember” is universally dismissed by critics as being full of errors and poorly plotted. The main character is a female novelist who struggles with memory loss while trying to solve a crime that happened in the past.

The professor told National Public Radio that when he read the book, he felt Christie was sensing what was happening to her, and that she kept writing “struck me as heroic.”

His study involved feeding the text of 16 of her novels into a computer program that analyzed the vocabulary for the frequency of different words and the number of different words in each novel. “The richness of the vocabulary of Christie’s novels declines with her age at composition. The three novels that she wrote in her 80s, (Nemesis, Elephants, and Postern of Fate,) have a smaller vocabulary than any of the analyzed works written by her between ages 28 to 63,” he writes.

Christie was 81 when she wrote the Elephants novel. Her use spiked of what Lancashire called indefinite words–”thing,” “anything,” “something,” “nothing.” At the same time, the number of different words Christie used dropped by 20 percent. “That is astounding,” Lancashire told NPR. “That is one-fifth of her vocabulary lost.”

Most of us don’t have large collections of writing done over the course of our lives. But Lancashire points out in his conclusion that “this will begin to change as more individuals begin to keep, if only by inertia, a lifetime archive of e-mail, blogs, professional documents, and the like.

“While the diversity of topics and genres in such an archive brings methodological problems to the analysis … we can nonetheless foresee the possibility of automated textual analysis as a part of the early diagnosis of Alzheimer’s disease and similar dementias.”

Lancashire’s paper, “Vocabulary Changes in Agatha Christie’s Mysteries as an Indication of Dementia: A Case Study.

The National Public Radio report.


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