Category: Alzheimer’s disease

n Alzheimer’s, Excess Tau Protein Damages Brain’s GPS and may be responsible for wandering

On By A.P.In Alzheimer's diseaseLeave a comment

Grid cell from the entorhinal cortex (EC) of the mouse brain, firing repeatedly and uniformly in a grid-like pattern. When a mouse moves through its environment, grid cells are activated, with each cell representing a specific location. This creates a triangular coordinate system that allows for spatial navigation. The accumulation of tau protein in the brain of a mouse model of Alzheimer’s disease was shown to disrupt the function of grid cells, causing problems with navigation. The findings explain why Alzheimer’s patients tend to wander and get lost. Source: Lab of Karen Duff, PhD, Columbia University Medical Center

Columbia University Medical Center (CUMC) researchers have discovered that the spatial disorientation that leads to wandering in many Alzheimer’s disease patients is caused by the accumulation of tau protein in navigational nerve cells in the brain. The findings, in mice, could lead to early diagnostic tests for Alzheimer’s and highlight novel targets for treating this common and troubling symptom.

The study was published online today in the journal Neuron.

An estimated three out of five people with Alzheimer’s disease wander and get lost, usually beginning in the early stages of the disease, leaving them vulnerable to injury. Researchers suspect that these problems originate in an area of the brain known as the entorhinal cortex (EC). The EC plays a key role in memory and navigation and is among the first brain structures affected by the buildup of neurofibrillary tangles that are largely composed of tau, a hallmark of Alzheimer’s disease. “Until now, no one has been able to show how tau pathology might lead to navigational difficulties,” said co-study leader Karen E. Duff, PhD, professor of pathology & cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at Columbia.

Dr. Duff and her colleagues focused their investigations on excitatory grid cells, a type of nerve cell in the EC that fires in response to movement through space, creating a grid-like internal map of a person’s environment. The researchers made electrophysiological recordings of the grid cells of older mice—including mice engineered to express tau in the EC (EC-tau mice) and normal controls—as they navigated different environments. Spatial cognitive tasks revealed that the EC-tau mice performed significantly worse compared to the controls, suggesting that tau alters grid cell function and contributes to spatial learning and memory deficits, according to co-study leader Abid Hussaini, PhD, assistant professor of neurobiology (in pathology & cell biology and the Taub Institute).

Detailed histopathological analysis of the mouse brains revealed that only the excitatory cells, but not the inhibitory cells, were killed or compromised by pathological tau, which probably resulted in the grid cells firing less. “It appears that tau pathology spared the inhibitory cells, disturbing the balance between excitatory and inhibitory cells and misaligning the animals’ grid fields,” said co-first author Hongjun Fu, PhD, associate research scientist in the Taub Institute, who led the immunohistological and behavior studies.

“This study clearly shows that tau pathology, beginning in the entorhinal cortex, can lead to deficits in grid cell firing and underlies the deterioration of spatial cognition that we see in human Alzheimer’s disease,” said Eric Kandel, MD, Nobel laureate, University Professor, and Kavli Professor of Brain Science at Columbia. “This is a classic advance in our understanding of the early stages of Alzheimer’s disease.”

“This study is the first to show a link between grid cells and Alzheimer’s disease,” said Edvard E. Moser, Nobel laureate and head of the Kavli Institute for Systems Neuroscience at Norwegian University of Science and Technology. “These findings will be crucial for future attempts to understand the development of early Alzheimer’s disease symptoms, including the tendency to wander and get lost.”

The findings raise the possibility that spatial disorientation could be treated by correcting this imbalance through transcranial stimulation, deep-brain stimulation, or light-based therapy.

“We have a lot to learn about grid cells and how they are affected by Alzheimer’s disease,” said Gustavo A. Rodriguez, PhD, a postdoctoral research scientist in the Taub Institute and a co-author of the paper. “We don’t yet know what percentage of healthy grid cells are needed for proper navigation or whether this system is rescuable once it has been compromised.”

“In the meantime,” said Dr. Duff, “our findings suggest that it may be possible to develop navigation-based cognitive tests for diagnosing Alzheimer’s disease in its initial stages. And if we can diagnose the disease early, we can start to give therapeutics earlier, when they may have a greater impact.”

The study is titled, “Tau Pathology Induces Excitatory Neuron Loss, Grid Cell Dysfunction and Spatial Memory Deficits Reminiscent of Early Alzheimer’s Disease.” The other contributors are Mathieu Herman, Sheina Emrani, Eden Nahmani, Geoffrey Barrett, Helen Y. Figueroa, and Eliana Goldberg.

The study was supported by grants from National Institutes of Health (R01NS074874 and R01AG050425) and the Alzheimer’s Association (2015-NIRG-341570).

http://newsroom.cumc.columbia.edu/blog/2017/01/19/in-alzheimers-excess-tau-protein-damages-brains-gps/

Having a socially interactive job helps protect from Alzheimer’s disease.

On By A.P.In Alzheimer's disease, brainLeave a comment

By Patrick Foster

Lawyers, teachers and doctors have a better chance of fighting off the effects of Alzheimer’s disease, because of the complex nature of their jobs, scientists reported this week.

Researchers found that people whose jobs combined complex thinking with social engagement with others – such as social workers and engineers – were better protected against the onset of Alzheimer’s, compared to those in manual work.

The study came as another report suggested that people with a poor diet could protect themselves against cognitive decline by adopting a mentally stimulating lifestyle.

Both pieces of research, published at the international conference of the Alzheimer’s Association, in Toronto, examined the impact of complex thinking on the onset of the disease.

In the first study, carried out by scientists at the Alzheimer’s Disease Research Centre, in Wisconsin, researchers examined white matter hyperintensities (WMHs) – white spots that appear on brain scans and are associated with Alzheimer’s – in 284 late-middle-aged patients considered at risk of contracting the disease.

They found that people who worked primarily with other people, as opposed to with “things or data”, were less likely to be affected by brain damage indicated by WMHs.

While lawyers, social workers, teachers and doctors were best protected, those who enjoyed the least protection included shelf-stackers, machine operators and labourers.

Elizabeth Boots, a researcher on the project, said: “These findings indicate that participants with higher occupational complexity are able to withstand pathology associated with Alzheimer’s and cerebrovascular disease and perform at a similar cognitive level as their peers.

“This association is primarily driven by work with people, rather than data or things. These analyses underscore the importance of social engagement in the work setting for building resilience to Alzheimer’s disease.”

The second study, carried out by Baycrest Health Sciences, in Toronto, examined the diet of 351 older adults.

Researchers found that those who had a traditional Western diet of red and processed meat, white bread, potatoes and sweets were more likely to experience cognitive decline.

However, those who adhered to such a diet but who had a mentally stimulating lifestyle enjoyed some protection from such decline.

Dr Matthew Parrott, one member of the team, said: “Our results show the role higher educational attainment, mentally stimulating work and social engagement can play in protecting your brain from cognitive decline, counteracting some negative effects of an unhealthy diet.

“This adds to the growing body of evidence showing how various lifestyle factors may combine to increase or protect against vulnerability to Alzheimer’s disease.”

Other research put forward at the convention included a study showing that digital brain training exercises can help stave of Alzheimer’s, and another paper that suggested that some newly-identified genes may also increase resilience to the disease.

Maria C. Carrillo, the chief science officer at the Alzheimer’s Association, said: “These new data add to a growing body of research that suggests more stimulating lifestyles, including more complex work environments with other people, are associated with better cognitive outcomes in later life.

“As each new study emerges, we further understand just how powerful cognitive reserve can be in protecting the brain from disease. Formal education and complex occupation could potentially do more than just slow cognitive decline – they may actually help compensate for the cognitive damage done by bad diet and small vessel disease in the brain.

“It is becoming increasingly clear that in addition to searching for pharmacological treatments, we need to address lifestyle factors to better treat and ultimately prevent Alzheimer’s and other dementias.”

http://www.telegraph.co.uk/news/2016/07/24/stressful-job-it-might-help-you-fight-off-alzheimers/

New treatment protocol shows promise of improving cognition in patients with Alzheimer’s disease

On By A.P.In Alzheimer's disease, DementiaLeave a comment

Ten patients with early Alzheimer’s disease or its precursors showed improvement in memory after treatment with Metabolic Enhancement for NeuroDegeneration (MEND), a programmatic and personalized therapy protocol.

Researchers described results from the small trial, which used quantitative MRI and neuropsychological testing of participants before and after treatment, in the study published online in Aging.

“ The magnitude of the improvement is unprecedented,” researchers wrote, “providing additional objective evidence that this programmatic approach to cognitive decline is highly effective.”

Before starting the program, the 10 participants had well-defined mild cognitive impairment, subjective cognitive impairment, or had been diagnosed with Alzheimer’s disease. Their subsequent treatment consisted of a complex, 36-point therapeutic personalized program that included comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

Researcher Dale Bredesen, MD, a professor at the Buck Institute for Research on Aging and at the Easton Laboratories for Neurodegenerative Disease Research at UCLA, Los Angeles, believes the protocol’s broader-based approach is key to its apparent success in reversing cognitive decline.

“Imagine having a roof with 36 holes in it, and your drug patched one hole very well — the drug may have worked, a single ‘hole’ may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much,” Dr. Bredesen said. “We think addressing multiple targets within the molecular network may be additive, or even synergistic, and that such a combinatorial approach may enhance drug candidate performance as well.”

Tests showed some participants “going from abnormal to normal,” Dr. Bredesen said.

In Aging , researchers describe the impact of MEND on all 10 patients, including:
•A 66-year-old man whose neuropsychological testing was compatible with a diagnosis of mild cognitive impairment. After 10 months on the MEND protocol, his hippocampal volume increased from the 17 th percentile for his age to the 75 th percentile, with an associated absolute increase in volume of nearly 12%.
•A 69-year-old entrepreneur with 11 years of progressive memory loss. After 22 months on the protocol, he showed marked improvements in all categories of neuropsychological testing, with long-term recall increasing from the 3 rd to 84 th percentile.
•A 49-year-old woman in the early stages of cognitive decline who, after 9 months on the protocol, no longer showed evidence on quantitative neuropsychological testing of cognitive decline.

Plans for larger studies are under way.

“Even though we see the far-reaching implications of this success,” Dr. Bredesen said, “we also realize that this is a very small study that needs to be replicated in larger numbers at various sites.”

http://www.psychcongress.com/article/mend-protocol-reverses-memory-loss-alzheimer%E2%80%99s-disease-27858

The Power of Music in Alleviating Dementia Symptoms

On By A.P.In Alzheimer's disease, brain, Dementia, Depression, Medicine, music, Neuropsychiatric DiseaseLeave a comment

by Tori Rodriguez, MA, LPC

As the search continues for effective drug treatments for dementia, patients and caregivers may find some measure of relief from a common, non-pharmaceutical source. Researchers have found that music-related memory appears to be exempt from the extent of memory impairment generally associated with dementia, and several studies report promising results for several different types of musical experiences across a variety of settings and formats.

“We can say that perception of music can be intact, even when explicit judgments and overt recognition have been lost,” Manuela Kerer, PhD, told Psychiatry Advisor. “We are convinced that there is a specialized memory system for music, which is distinct from other domains, like verbal or visual memory, and may be very resilient against Alzheimer’s disease.”

Kerer is a full-time musical composer with a doctoral degree in psychology who co-authored a study on the topic while working at the University of Innsbruck in Austria. She and her colleagues investigated explicit memory for music among ten patients with early-state Alzheimer’s disease (AD) and ten patients with mild cognitive impairment (MCI), and compared their performance to that of 23 healthy participants. Not surprisingly, the patient group demonstrated worse performance on tasks involving verbal memory, but they did significantly better than controls on the music-perceptional tasks of detecting distorted tunes and judging timbre.

“The temporal brain structures necessary for verbal musical memory were mildly affected in our clinical patients, therefore attention might have shifted to the discrimination tasks which led to better results in this area,” she said. “Our results enhance the notion of an explicit memory for music that can be distinguished from other types of explicit memory — that means that memory for music could be spared in this patient group.”

Other findings suggest that music might even improve certain aspects of memory among people with dementia. In a randomized controlled trial published in last month in the Journal of Alzheimer’s Disease, music coaching interventions improved multiple outcomes for both patients with dementia and their caregivers. The researchers divided 89 pairs of patients with dementia and their caregivers into three groups: two groups were assigned to caregiver-led interventions that involved either singing or listening to music, while a third group received standard care. Before and after the 10-week intervention, and six months after the intervention, participants were assessed on measures of mood, quality of life and neuropsychological functioning.

Results showed that the singing intervention improved working memory among patients with mild dementia and helped to preserve executive function and orientation among younger patients, and it also improved the well-being of caregivers. The listening intervention was found to have a positive impact on general cognition, working memory and quality of life, particularly among patients in institutional care with moderate dementia not caused by AD. Both interventions led to reductions in depression.

The findings suggest that “music has the power to improve mood and stimulate cognitive functions in dementia, most likely by engaging limbic and medial prefrontal brain regions, which are often preserved in the early stages of the illness,” study co-author Teppo Särkämö, PhD, a researcher at the University of Helsinki, Finland, told Psychiatry Advisor. “The results indicate that when used regularly, caregiver-implemented musical activities can be an important and easily applicable way to maintain the emotional and cognitive well-being of persons with dementia and also to reduce the psychological burden of family caregivers.”

Singing has also been shown to increase learning and retention of new verbal material in patients with AD, according to research published this year in the Journal of Clinical & Experimental Neuropsychology, and findings published in 2013 show that listening to familiar music improves the verbal narration of autobiographical memories in such patients. Another study found that a music intervention delivered in a group format reduced depression and delayed the deterioration of cognitive functions, especially short-term recall, in patients with mild and moderate dementia. Group-based music therapy appears to also decrease agitation among patients in all stages of dementia, as described in a systematic review published in 2014 in Nursing Times.

n addition to the effects of singing and listening to music on patients who already have dementia, playing a musical instrument may also offer some protection against the condition, according to a population-based twin study reported in 2014 in the International Journal of Alzheimer’s Disease. Researchers at the University of Southern California found that older adults who played an instrument were 64% less likely than their non-musician twin to develop dementia or cognitive impairment.

“Playing an instrument is a unique activity in that it requires a wide array of brain regions and cognitive functions to work together simultaneously, throughout both the right and left hemispheres,” co-author Alison Balbag, PhD, told Psychiatry Advisor. While the study did not examine causal mechanisms, “playing an instrument may be a very effective and efficient way to engage the brain, possibly granting older musicians better maintained cognitive reserve and possibly providing compensatory abilities to mitigate age-related cognitive declines.”

She notes that clinicians might consider suggesting that patients incorporate music-making into their lives as a preventive activity, or encouraging them to keep it up if they already play an instrument.
Further research, particularly neuroimaging studies, is needed to elucidate the mechanisms behind the effects of music on dementia, but in the meantime it could be a helpful supplement to patients’ treatment plans. “Music has considerable potential and it should be introduced much more in rehabilitation and neuropsychological assessment,” Kerer said.

http://www.psychiatryadvisor.com/alzheimers-disease-and-dementia/neurocognitive-neurodegenerative-memory-musical-alzheimers/article/452120/3/

References

Kerer M, Marksteiner J, Hinterhuber H, et al. Explicit (semantic) memory for music in patients with mild cognitive impairment and early-stage Alzheimer’s disease. Experimental Aging Research; 2013; 39(5):536-64.

Särkämö T, Laitinen S, Numminen A, et al. Clinical and Demographic Factors Associated with the Cognitive and Emotional Efficacy of Regular Musical Activities in Dementia. Journal of Alzheimer’s Disease; 2015; published online ahead of print.

Palisson J, Roussel-Baclet C, Maillet D, et al. Music enhances verbal episodic memory in Alzheimer’s disease. Journal of Clinical & Experimental Neuropsychology; 2015; 37(5):503-17.

El Haj M, Sylvain Clément, Luciano Fasotti, Philippe Allain. Effects of music on autobiographical verbal narration in Alzheimer’s disease. Journal of Neurolinguistics; 2013; 26(6): 691–700.

Chu H, Yang CY, Lin Y, et al. The impact of group music therapy on depression and cognition in elderly persons with dementia: a randomized controlled study. Biological Research for Nursing; 2014; 16(2):209-17.

Craig J. Music therapy to reduce agitation in dementia. Nursing Times; 2014; 110(32-33):12-5.
Balbag MA, Pedersen NL, Gatz M. Playing a Musical Instrument as a Protective Factor against Dementia and Cognitive Impairment: A Population-Based Twin Study. International Journal of Alzheimer’s Disease; 2014; 2014: 836748.

New research shows that people with ‘O’ blood type have decreased risk of cognitive decline

On By A.P.In Alzheimer's disease, brain, Dementia, Medicine, Neuropsychiatric Disease, Science, The BrainLeave a comment

A pioneering study conducted by leading researchers at the University of Sheffield has revealed blood types play a role in the development of the nervous system and may impact the risk of developing cognitive decline.

The research, carried out in collaboration with the IRCCS San Camillo Hospital Foundation in Venice, shows that people with an ‘O’ blood type have more grey matter in their brain, which helps to protect against diseases such as Alzheimer’s, than those with ‘A’, ‘B’ or ‘AB’ blood types.

Research fellow Matteo De Marco and Professor Annalena Venneri, from the University’s Department of Neuroscience, made the discovery after analysing the results of 189 Magnetic Resonance Imaging (MRI) scans from healthy volunteers.

The researchers calculated the volumes of grey matter within the brain and explored the differences between different blood types.

The results, published in the Brain Research Bulletin, show that individuals with an ‘O’ blood type have more grey matter in the posterior proportion of the cerebellum.

In comparison, those with ‘A’, ‘B’ or ‘AB’ blood types had smaller grey matter volumes in temporal and limbic regions of the brain, including the left hippocampus, which is one of the earliest part of the brain damaged by Alzheimer’s disease.

These findings indicate that smaller volumes of grey matter are associated with non-‘O’ blood types.

As we age a reduction of grey matter volumes is normally seen in the brain, but later in life this grey matter difference between blood types will intensify as a consequence of ageing.

“The findings seem to indicate that people who have an ‘O’ blood type are more protected against the diseases in which volumetric reduction is seen in temporal and mediotemporal regions of the brain like with Alzheimer’s disease for instance,” said Matteo DeMarco.

“However additional tests and further research are required as other biological mechanisms might be involved.”

Professor Annalena Venneri added: “What we know today is that a significant difference in volumes exists, and our findings confirm established clinical observations. In all likelihood the biology of blood types influences the development of the nervous system. We now have to understand how and why this occurs.”

More information: “‘O’ blood type is associated with larger grey-matter volumes in the cerebellum,” Brain Research Bulletin, Volume 116, July 2015, Pages 1-6, ISSN 0361-9230, dx.doi.org/10.1016/j.brainresbull.2015.05.005

Biogen Reports Its Alzheimer’s Drug Sharply Slowed Cognitive Decline

On By A.P.In Alzheimer's disease, Medicine, Neuropsychiatric DiseaseLeave a comment

An experimental drug for Alzheimer’s disease sharply slowed the decline in mental function in a small clinical trial, researchers reported Friday, reviving hopes for an approach to therapy that until now has experienced repeated failures.

The drug, being developed by Biogen Idec, could achieve sales of billions of dollars a year if the results from the small trial are replicated in larger trials that Biogen said it hoped to begin this year. Experts say that there are no really good drugs now to treat Alzheimer’s.

Biogen’s stock has risen about 50 percent since early December, when the company first announced that the drug had slowed cognitive decline in the trial, without saying by how much. Analysts and investors had been eagerly awaiting the detailed results, some of them flying to France to hear Biogen researchers present them at a neurology meeting on Friday.

The drug, called aducanumab, met and in some cases greatly exceeded Wall Street expectations in terms of how much the highest dose slowed cognitive decline. However, there was a high incidence of a particular side effect that might make it difficult to use the highest dose.

Still, the net impression was positive. “Out-of-the-ballpark efficacy, acceptable safety,” Ravi Mehrotra, an analyst at Credit Suisse, wrote on Friday. Shares of Biogen rose $42.33, or 10 percent, to $475.98.

Alzheimer’s specialists were impressed, but they cautioned that it was difficult to read much from a small early-stage, or Phase 1, trial that was designed to look at safety, not the effect on cognition. Also, other Alzheimer’s drugs that had looked promising in early studies ended up not working in larger trials.

“It’s certainly encouraging,” said Dr. Samuel Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York, who was not involved in the study. He said the effect of the highest dose was “pretty impressive.”

Aducanumab, which until now has been called BIIB037, is designed to get rid of amyloid plaque in the brain, which is widely believed to be a cause of the dementia in Alzheimer’s disease. However, other drugs designed to prevent or eliminate plaque have failed in large clinical trials, raising questions about what role the plaque really plays.

Johnson & Johnson and Pfizer abandoned a drug they were jointly developing after it showed virtually no effect in large trials. Eli Lilly and Roche are continuing to test their respective drugs despite initial failures. Experts say there is some suggestion the drugs might work if used early enough, when the disease is still mild.

Biogen tried to increase its chances of success by treating patients with either mild disease or so-called prodromal disease, an even earlier stage. It also enrolled only patients shown to have plaque in their brains using a new imaging technique. In some trials of other drugs, some of the patients turned out not to have plaque, which could have been a reason the trials were not successful.

The results reported Friday were for 166 patients, who were randomly assigned to get one of several doses of the drug or a placebo. The drug not only slowed cognitive decline but also substantially reduced plaque in the brain, and higher doses were better than lower doses. Those are signs that the effects seen were from the drug.

“It would be kind of hard to get those kind of results by chance,” said Dr. Rachelle S. Doody, director of the Alzheimer’s Disease and Memory Disorders Center at Baylor College of Medicine, who was not involved in the study but has been a consultant to Biogen and many other companies.

On one measure of cognition, a 30-point scale called the mini-mental state exam or M.M.S.E., those receiving the placebo worsened by an average of 3.14 points over the course of a year. The decline at one year was only 0.58 points for those getting the highest dose and 0.75 points for a middle dose. The difference with a placebo was statistically significant for both doses.

On another measure of both cognition and the ability to function in daily tasks, patients in the placebo group worsened by an average of 2.04 points at one year. Those getting the highest dose of the drug had a decline of only 0.59, a statistically significant difference.

Some analysts said they would have been impressed if the drug had slowed the rate of cognitive decline by 20 or 30 percent. But the actual reduction for the high dose was above 70 percent. They said the drug’s effect was stronger than that of Lilly’s drug.

A major side effect was a localized swelling in the brain, known as A.R.I.A.-E. This has been seen with other drugs in this class, though the rate for aducanumab seems higher.

Among patients with a genetic variant that raises the risk of getting Alzheimer’s, 55 percent of those who got the highest dose suffered this side effect, and about 35 percent of the high-dose patients dropped out of the trial because of this. Among those without the genetic variant, 17 percent of those who got the highest dose suffered the side effect and 8 percent discontinued treatment.

Biogen said the swelling often did not cause symptoms and probably could be managed by watching for it and reducing doses. Dr. Doody and Dr. Gandy agreed.

But Dr. Thomas M. Wisniewski, a professor of neurology at NYU Langone Medical Center, disagreed. “Most clinicians would find that unacceptable,” he said in a conference call hosted by the Wall Street firm Evercore ISI. He said the side effect was “something you definitely don’t want happening in your patients.”

Over all, however, Dr. Wisniewski was enthusiastic, saying the drug looked to be “way better” than Lilly’s.

A lesser dose might suffice. There were no discontinuations from this side effect among patients taking a middle dose. And that middle dose also seemed somewhat effective in slowing cognitive decline.

The results were presented in Nice, France, at the International Conference on Alzheimer’s and Parkinson’s Diseases and Related Neurological Disorders.

Depression, Behaviour Changes May Start in Alzheimer’s Even Before Memory Changes

On By A.P.In Alzheimer's disease, Dementia, Depression, Medicine, Neuropsychiatric DiseaseLeave a comment

Depression and other behaviour changes may show up in people who will later develop Alzheimer’s disease even before they start having memory problems, according to a study published in the January 14, 2015, online issue of the journal Neurology.

“While earlier studies have shown that an estimated 90% of people with Alzheimer’s experience behavioural or psychological symptoms such as depression, anxiety, and agitation, this study suggests that these changes begin before people even have diagnosable dementia,” said Catherine M. Roe, PhD, Washington University School of Medicine, St. Louis, Missouri.

The study looked at 2,416 people aged 50 years and older who had no cognitive problems at their first visit to one of 34 Alzheimer’s disease centres across the country. The participants were followed for up to 7 years. Of the participants, 1,198 people stayed cognitively normal, with no memory or thinking problems, during the study. They were compared with 1,218 people who were followed for about the same length of time, but who developed dementia.

The people who developed dementia during the study also developed behaviour and mood symptoms such as apathy, appetite changes, irritability, and depression sooner than the people who did not develop dementia. For example, 30% of people who would develop dementia had depression after 4 years in the study, compared with 15% of those who did not develop dementia. Those who developed dementia were more than twice as likely to develop depression sooner than those without dementia and more than 12 times more likely to develop delusions than those without dementia.

Dr. Roe said the study adds to the conflicting evidence on depression and dementia.

“We still don’t know whether depression is a response to the psychological process of Alzheimer’s disease or a result of the same underlying changes in the brain,” she said. “More research is needed to identify the relationship between these two conditions.”

http://dgnews.docguide.com/depression-behaviour-changes-may-start-alzheimer-s-even-memory-changes?overlay=2&nl_ref=newsletter&pk_campaign=newsletter

Glen Campbell releases powerful final song and video about his future with Alzheimer’s disease

On By A.P.In Alzheimer's disease, Medicine, music, Neuropsychiatric DiseaseLeave a comment

I’m still here, but yet I’m gone
I don’t play guitar or sing my songs
They never defined who I am
The man that loves you ’til the end
You’re the last person I will love
You’re the last face I will recall
And best of all, I’m not gonna miss you.
Not gonna miss you.
I’m never gonna hold you like I did
Or say I love you to the kids
You’re never gonna see it in my eyes
It’s not gonna hurt me when you cry
I’m never gonna know what you go through
All the things I say or do
All the hurt and all the pain
One thing selfishly remains
I’m not gonna miss you
I’m not gonna miss you

The Country Music Hall of Fame member, who was diagnosed with Alzheimer’s disease in 2011, is out with the video for the final song he’ll ever record — “I’m Not Gonna Miss You.” It was recorded in 2013 with producer Julian Raymond.

“I’m still here but yet I’m gone/ I don’t play guitar or sing my songs,” the tune begins as it details his struggles with the disease.

The poignant music video that accompanies it spans Campbell’s career. It contrasts Campbell singing in the studio with home video and clips from throughout his career. There are even images of doctors discussing his brain scans with him.

Because of the progression of the disease, the 78-year-old Campbell was admitted to a special care facility in Nashville in April.

“Sadly, Glen’s condition has progressed enough that we were no longer able to keep him at home,” Campbell’s family said in a statement to Rolling Stone. “He is getting fantastic care and we get to see him every day. Our family wants to thank everyone for their continued prayers, love and support.”

Campbell, who was inducted into the Country Music Hall of Fame in 2005 and is best known for his hits like “Rhinestone Cowboy” and “Wichita Lineman,” took his Alzheimer’s in stride.

“I just take it as it comes, you know,” Campbell said in a CNN interview in February 2012. “I know that I have a problem with that (forgetfulness), but it doesn’t bother me. If you’re going to have it handed to you, you have got to take it, anyway. So that is the way I look at it.”

In a career that spans five decades, he released his final album “Ghost on Canvas” in 2011 and then went on a farewell tour.

http://www.cnn.com/2014/10/14/showbiz/glen-campbell-final-song/index.html?hpt=hp_c2

New blood test to predict who will develop Alzheimer’s disease

On By A.P.In Alzheimer's disease, Georgetown University Medical Center, Howard Federoff, Mark Mapstone, Nature Medicine, neurologist, Neurology, Neuropsychiatric Disease, Neuroscience, neuroscientist, Science, The Brain, University of Rochester Medical Center in New YorkLeave a comment

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In a first-of-its-kind study, researchers have developed a blood test for Alzheimer’s disease that predicts with astonishing accuracy whether a healthy person will develop the disease.

Though much work still needs to be done, it is hoped the test will someday be available in doctors’ offices, since the only methods for predicting Alzheimer’s right now, such as PET scans and spinal taps, are expensive, impractical, often unreliable and sometimes risky.

“This is a potential game-changer,” said Dr. Howard Federoff, senior author of the report and a neurologist at Georgetown University Medical Center. “My level of enthusiasm is very high.”

The study was published in Nature Medicine.

In the beginning, the researchers knew they wanted to find a blood test to detect Alzheimer’s but didn’t know what specifically to look for. Should they examine patients’ DNA? Their RNA? Or should they look for the byproducts of DNA and RNA, such as fats and proteins?

They decided to start with fats, since it was the easiest and least expensive. They drew blood from hundreds of healthy people over age 70 living near Rochester, New York, and Irvine, California. Five years later, 28 of the seniors had developed Alzheimer’s disease or the mild cognitive problems that usually precede it.

Scouring more than 100 fats, or lipids, for what might set this group apart, they found that these 28 seniors had low levels of 10 particular lipids, compared with healthy seniors.

To confirm their findings, the researchers then looked at the blood of 54 other patients who had Alzheimer’s or mild cognitive impairment. This group also had low levels of the lipids.

Overall, the blood test predicted who would get Alzheimer’s or mild cognitive impairment with over 90% accuracy.

“We were surprised,” said Mark Mapstone, a neuropsychologist at the University of Rochester Medical Center and lead author of the study. “But it turns out that it appears we were looking in the right place.”

The beauty of this test, Mapstone says, is that it caught Alzheimer’s before the patient even had symptoms, suggesting that the disease process begins long before people’s memories start failing. He says that perhaps the lipid levels started decreasing at the same time as brain cells started dying.

He and his team plan to try out this test in people in their 40s and 50s. If that works, he says, that would be the “holy grail,” because then researchers could try experimental drugs and treatments in a group that’s almost sure to get the disease. That would speed research along immensely.

Plus, people could get a heads up that they were probably destined to get Alzheimer’s. Although some people might not want to know that they’re destined for a horrible disease, others might be grateful for the warning.

Federoff said he would want to know whether he was on his way to getting the disease, even though there’s nothing he could do about it. He might want to take a family trip he’d been thinking about or might want to appoint a successor at work.

“I would make sure that things that are important to me get done,” he said.

But, Federoff added, others might not want to know they were about to get a devastating disease they were powerless to stop.

“I think it’s a very personal decision,” Federoff said. “It would have to be thought through on multiple dimensions. Patients and their families would have to be counseled.”

Other research teams are looking at other possible tests for Alzheimer’s. The need for a screening test of some kind for Alzheimer’s has never been greater: A report released last week says the disease claims the lives of perhaps a half a million Americans, making it nearly as deadly as heart disease and cancer.

If any of these tests work out — and that’s still an if — it would take years to make it to doctors’ offices, since the test would need to be validated by other labs and with larger groups of people. Thee test developed by the Georgetown and Rochester researchers, for example, was used mainly in white people, and it might not work as well with other groups.

Heather Snyder, a spokeswoman for the Alzheimer’s Association, said the study was well done but much work is still needed.

“It’s an interesting paper. It’s an intriguing study. But it is very preliminary,” she said.http://www.cnn.com/2014/03/09/health/alzheimers-blood-test/index.html?hpt=hp_t2

New research shows that sleep functions to allow the brain to eliminate toxins that accumulate while we are awake

On By A.P.In Alzheimer's disease, beta amyloid, brain, brain cleaning, Kebmodee, Maiken Nedergaard, Medicine, mental concentration, mental health, mental illness, National Institute of Neurological Disorders and Stroke, neurologist, Neurology, Neuropsychiatric Disease, Neuroscience, NINDS, Randall Bateman, Science, University of Rochester, Washington UniversityLeave a comment

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While the brain sleeps, it clears out harmful toxins, a process that may reduce the risk of Alzheimer’s, researchers say.

During sleep, the flow of cerebrospinal fluid in the brain increases dramatically, washing away harmful waste proteins that build up between brain cells during waking hours, a study of mice found.

“It’s like a dishwasher,” says Dr. Maiken Nedergaard, a professor of neurosurgery at the University of Rochester and an author of the study in Science.

The results appear to offer the best explanation yet of why animals and people need sleep. If this proves to be true in humans as well, it could help explain a mysterious association between sleep disorders and brain diseases, including Alzheimer’s.

Nedergaard and a team of scientists discovered the cleaning process while studying the brains of sleeping mice. The scientists noticed that during sleep, the system that circulates cerebrospinal fluid through the brain and nervous system was “pumping fluid into the brain and removing fluid from the brain in a very rapid pace,” Nedergaard says.

The team discovered that this increased flow was possible in part because when mice went to sleep, their brain cells actually shrank, making it easier for fluid to circulate. When an animal woke up, the brain cells enlarged again and the flow between cells slowed to a trickle. “It’s almost like opening and closing a faucet,” Nedergaard says. “It’s that dramatic.”

Nedergaard’s team, which is funded by the National Institute of Neurological Disorders and Stroke, had previously shown that this fluid was carrying away waste products that build up in the spaces between brain cells.

The process is important because what’s getting washed away during sleep are waste proteins that are toxic to brain cells, Nedergaard says. This could explain why we don’t think clearly after a sleepless night and why a prolonged lack of sleep can actually kill an animal or a person, she says.

So why doesn’t the brain do this sort of housekeeping all the time? Nedergaard thinks it’s because cleaning takes a lot of energy. “It’s probably not possible for the brain to both clean itself and at the same time [be] aware of the surroundings and talk and move and so on,” she says.

The brain-cleaning process has been observed in rats and baboons, but not yet in humans, Nedergaard says. Even so, it could offer a new way of understanding human brain diseases including Alzheimer’s. That’s because one of the waste products removed from the brain during sleep is beta amyloid, the substance that forms sticky plaques associated with the disease.

That’s probably not a coincidence, Nedergaard says. “Isn’t it interesting that Alzheimer’s and all other diseases associated with dementia, they are linked to sleep disorders,” she says.

Researchers who study Alzheimer’s say Nedergaard’s research could help explain a number of recent findings related to sleep. One of these involves how sleep affects levels of beta amyloid, says Randall Bateman, a professor of neurology Washington University in St. Louis who wasn’t involved in the study.

“Beta amyloid concentrations continue to increase while a person is awake,” Bateman says. “And then after people go to sleep that concentration of beta amyloid decreases. This report provides a beautiful mechanism by which this may be happening.”

The report also offers a tantalizing hint of a new approach to Alzheimer’s prevention, Bateman says. “It does raise the possibility that one might be able to actually control sleep in a way to improve the clearance of beta amyloid and help prevent amyloidosis that we think can lead to Alzheimer’s disease.”

http://www.npr.org/blogs/health/2013/10/17/236211811/brains-sweep-themselves-clean-of-toxins-during-sleep

http://m.sciencemag.org/content/342/6156/373.abstract

Thanks to Kebmodee for bringing this to the It’s Interesting community.