Tag: dementia

Adding lithium to tap water may decrease rates of dementia

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by CHRIS SMYTH

People living in areas with high levels of lithium in tap water are 17 per cent less likely to get dementia, according to a large study that suggests the naturally occurring metal could help to prevent mental decline.

The findings raise the possibility that lithium could one day be added to drinking water to protect the brain in the same way as fluoride is added to protect teeth.

Lithium is already widely available as a psychiatric drug and experts said the findings suggested that it could be used as a treatment to prevent dementia if further trials proved successful. Lithium is known to affect neurological signalling and has long been used as a treatment for conditions such as bipolar disorder. It occurs naturally in water and previous studies have found lower suicide rates in areas with higher levels.

Scientists studied 74,000 older people with dementia and 734,000 without across Denmark, comparing illness rates with lithium levels, which were 15 times higher in some areas.

Scientists at the University of Copenhagen found that dementia rates increased slightly with low levels of lithium before falling sharply above 10 micrograms per litre. At 15 to 27 micrograms/l, dementia rates were 17 per cent lower than for 2-5 micrograms/l, according to results published in JAMA Psychiatry.

The authors acknowledged that other factors could explain the results, including worse healthcare in the remoter areas that had less lithium in water, but they said it was plausible that tiny amounts in tap water could have a significant effect on dementia.

In a linked editorial John McGrath, of the University of Queensland, and Michael Berk, of the University of Melbourne, wrote: “In the spirit of alchemy, could we convert lithium, a simple metal used as a mood stabiliser, into a golden public health intervention that could prevent dementia?

They added: “That a relatively safe, simple, and cheap intervention (ie optimising lithium concentrations in the drinking water) could lead to the primary prevention of dementia is a tantalising prospect.”

David Smith, emeritus professor of pharmacology at the University of Oxford, said the findings tallied with MRI studies showing that lithium salts increased the volume of areas of the brain involved in Alzheimer’s. However, he added: “We should not be adding lithium salts to our tap water because we would not know what amount to use.”

David Reynolds, chief scientific officer at Alzheimer’s Research UK, said: “It is potentially exciting that low doses of a drug already available in the clinic could help limit the number of people who develop dementia.”

Rob Howard, professor of old-age psychiatry at University College London, said: “These results represent another important piece of evidence for lithium’s potential as a treatment for Alzheimer’s disease. We now need clinical trials of lithium in patients with Alzheimer’s disease to determine once and for all whether this cheap and well-tolerated element can slow dementia progression.”

http://www.theaustralian.com.au/news/world/the-times/lithium-in-tap-water-could-lower-dementia-risk/news-story/c40599203eca195402c03c0a168961a6

Increasing muscle strength through weight resistance training improves cognitive function and may prevent dementia

On By A.P.In aged brain, ageing, aging1 Comment

In Australia, a University of Sydney study has linked improved cognitive function with stronger muscles using a steady regime of weightlifting exercises. Published in the Journal of American Geriatrics, the study used a system known as SMART (Study of Mental and Resistance Training). A trial was done on a group of patients age 55 to 68, suffering MCI (mild cognitive impairment). This condition is not as serious as full-blown dementia, as people affected only have mild cognitive symptoms not severe enough to disable them from normal daily life.

People who have MCI though are at high risk of developing dementia or Alzheimer’s with 80% going on to develop Alzheimer’s disease within 6 years. The World Alzheimer Report 2016 has reported that 47 million people globally are affected by dementia related diseases, with an expected three-fold increase by the year 2050. The cost of care is high for these patients, with a focus only on extending the quality of life for those living with dementia.

Weight Training Improves Cognitive Functions

The aim of the study was to measure the effects of different physical and mental activities on the human brain. Researchers examined 100 people affected by MCI. They were divided into four groups, and assigned the activities as seen below:
•weightlifting exercises
•seated stretching exercises
•real cognitive training on a computer
•placebo training on a computer

The weightlifting trial lasted for 6 months with exercising done twice a week. As the participants got stronger, they increased the amount of weight for each exercise. The exercises were done while trying to maintain 80% or greater at their peak strength.

Surprisingly, only the weight training activity demonstrated a measured improvement in brain function. The stretching exercises, cognitive training, and placebo training did not yield any results. This proved a link between muscle strength gained through physical training and the improved cognitive functions. According to Doctor Yorgi Mavros, lead author of the study, there was a clear relationship between mental functions and increased muscular strength. And the stronger the muscles got the greater the mental improvement.

In an earlier study, researchers scanned the brains of older adults after 6 months of weight training. The results mirrored the SMART trial with measured brain growth. Although previous studies have been done that show links between exercise and improved brain functions, the SMART system went into detail on the types of exercise required to get the best results. This study was a first in showing evidence of a link between strength training and improved cognitive functions for people with MCI who were 55 or older.

Delaying or Stopping Aging in the Brain

People increase their chances of brain impairment by not exercising. Exercise can help prevent dementia and Alzheimer’s disease, but also improves cardiovascular health and some other cognitive processes like multitasking.

Doctor Mavros is a strong advocate for encouraging resistance exercises as people start to grow older. The result could be a much healthier aging population. Mavros stressed the need for exercising at least 2-3 time per week at a high enough intensity in order to get the maximum cognitive benefits.

Professor Maria Fiatarone Singh of the University of Sydney wants to discover the underlying process of muscle growth and brain growth and its effect on cognitive performance. The next step is deciding how to prescribe optimal exercise programs to individuals with mild cognitive impairment, and to those who want to prevent MCI.

The authors of the study pointed out that the mechanism behind weight training and improving cognitive impairment has not yet been determined and future study may uncover the secret of delaying or even stopping degenerative aging effects of the brain.

http://www.worldhealth.net/news/stronger-muscles-improved-cognitive-function/

Caffeine may help protect older women from dementia

On By A.P.In DementiaLeave a comment

In a large group of older women, those who consumed higher amounts of caffeine had lower rates of incident dementia than those who consumed lower amounts over as many as 10 years of follow-up in a study. Researchers published their findings in The Journals of Gerontology.

“The mounting evidence of caffeine consumption as a potentially protective factor against cognitive impairment is exciting given that caffeine is also an easily modifiable dietary factor with very few contraindications,” said study lead author Ira Driscoll, PhD, a professor of psychology at the University of Wisconsin-Milwaukee. “What is unique about this study is that we had an unprecedented opportunity to examine the relationships between caffeine intake and dementia incidence in a large and well-defined, prospectively-studied cohort of women.”

The findings are based on 6467 community-dwelling women age 65 and older who self-reported their daily caffeine consumption upon enrollment in the Women’s Health Initiative Memory Study, which is funded by the National Heart, Lung, and Blood Institute.

Over up to a decade of follow-up, the women received annual assessments of cognitive function, and 388 of them were diagnosed with probable dementia or some form of cognitive impairment.

After adjusting for a number of risk factors including age, hormone therapy, sleep quality, and depression, researchers found that women who consumed above-average levels of caffeine (more than 261 mg per day) were 36% less likely to develop incident dementia. To provide perspective, the study explained that an 8-ounce cup of coffee contains 95 mg of caffeine, 8 ounces of brewed black tea contains 47 mg, and a 12-ounce can of cola contains 33 mg.

“Our findings suggest lower odds of probable dementia or cognitive impairment in older women whose caffeine consumption was above median for this group,” the researchers concluded, “and are consistent with the existing literature showing an inverse association between caffeine intake and age-related cognitive impairment.”

—Jolynn Tumolo

References

Driscoll I, Shumaker SA, Snively BM, et al. Relationships between caffeine intake and risk for probable dementia or global cognitive impairment: the Women’s Health Initiative Memory Study. The Journals of Gerontology. 2016 September 27;[Epub ahead of print].

Viral and Bacterial Links to the Brain’s Decline

On By A.P.In brainLeave a comment


Herpes simplex viruses pass through the outer protein coat of a nucleus, magnified 40,000 times. Dr. Ruth Itzhak’s research published in 1997 revealed a potential link to the presence of HSV-1 (one specific variety of Herpes simplex) and the onset of Alzheimer’s in 60 percent of the cases they studied. However, she has only been able to study a low number of cases since the work has received only a cursory nod from the greater research world and little funding.

By Ed Cara

As recently as the 1970s, doctors stubbornly treated complaints of festering open sores in the stomach as a failing of diet or an inability to manage stress. Though we had long accepted the basic premise of Louis Pasteur’s germ theory—that flittering short bursts of disease and death are often caused by microscopic beings that could be stopped by sanitary food, water and specially crafted drugs—many researchers ardently resisted the idea that they could also trigger more complicated, chronic illnesses.

When it came to ulcers, no one believed that any microorganisms could endure in the acidic cauldron of our digestive system. It took the gumshoe work of Australian doctors and medical researchers Barry Marshall and Robin Warren in the 1980s to debunk that belief and discover the specific bug responsible for most chronic stomach ulcers, Helicobacter pylori. Marshall even went so far as to swallow the germ to prove the link was real and, obviously, became sick soon after. Thankfully, his self-sacrifice was eventually validated when he and Warren were awarded a Nobel Prize in 2005.

But while modern medicine has grown comfortable with the idea that even chronic physical ailments can be sparked by the living infinitesimal, there is an even bolder, more controversial proposition from a growing number of researchers. It’s the idea that certain germs, bugs and microbes can lie hidden in the body for decades, all the while slowly damaging our brains, even to the point of dementia, depression and schizophrenia.

In January 2016, a team led by Shawn Gale, an associate professor in psychology at Brigham Young University, looked at the infection history of 5,662 young to middle-aged adults alongside the results of tests intended to measure cognition. Gale’s rogues’ gallery included both parasites (the roundworm and Toxoplasma gondii ) and viruses (the hepatitis clan, cytomegalovirus, and herpes simplex virus Types 1 and 2). The team created an index of infectious disease —the more bugs a participant had been exposed to, the higher the person’s index score. It turned out that those with a higher score were more likely to have worse learning and memory skills, as well as slower information-processing speed than those with a lower score, even after controlling for other factors, like age, sex and financial status.

Aside from their shared ability to stay rooted inside us, the ways these pathogens might influence our noggins are as varied as their biology is from one another. Some, like T. gondii (often transmitted to humans via contaminated cats and infected dirt), can discreetly infest the brain and cause subtle changes to our brain chemistry, altering levels of neurotransmitters like dopamine while causing no overt signs of disease. Others, like hepatitis C, are suspected of hitching a ride onto infected white blood cells that cross the brain-blood barrier and, once inside, deplete our supply of white brain matter, the myelin-coated axons that help neurons communicate with each other and seem to actively shape how we learn. And still others, like H. pylori, could trigger a low-level but chronic inflammatory response that gradually wears down our body and mind alike.

Gale’s team found only fairly small deficits in cognition connected to infection. But other researchers, like Ruth Itzhaki, professor emeritus of molecular neurobiology at Britain’s University of Manchester, believe microbes may play an outsized role in one of the most devastating neurodegenerative disorders around: Alzheimer’s disease, which afflicted 47 million people worldwide in 2015. Last March, Itzhaki and a globe-spanning group of researchers penned an editorial in the Journal of Alzheimer’s Disease, imploring the scientific community to more seriously pursue a proposed link between Alzheimer’s and particular germs, namely herpes simplex virus Type 1 (HSV-1), Chlamydia pneumoniae and spirochetes—a diverse group of bacteria that include those responsible for syphilis and Lyme disease. The unusually direct plea, for scientists at least, was the culmination of decades of frustration.

“There’s great hostility to the microbial concept amongst certain influential people in the field, and they are the ones who usually determine whether or not one’s research grant application is successful,” says Itzhaki. “The irony is that they never provide scientific objections to the concepts—they just belittle them, so there’s nothing to rebut!”

It’s a frustration Itzhaki knows too well; in 1991, her lab published the first paper finding a clear HSV-1 link to Alzheimer’s. Since then, according to Itzhaki, over 100 published studies, from her lab and elsewhere, have been supportive of the same link. Nevertheless, Itzhaki says, the work has received only a cursory nod from the greater research world and little funding. Out of the $589 million allocated to Alzheimer’s research by the National Institutes of Health in 2015, exactly zero appeared to be spent on studying the proposed HSV-1 connection.

HSV-1 is more often known as the version of herpes that causes cold sores. Nearly all of us carry the virus from infancy; our peripheral nervous system serves as its dormant nesting ground. From there, HSV-1 can reactivate and occasionally cause mild flare-ups of disease, typically when our immune system is overwhelmed due to stress or other infections. Itzhaki’s lab, however, found that by the time we reach our golden years, the virus often migrates to the brain, where it remains capable of resurrecting itself and wreaking a new sort of havoc when opportunity presents, such as when our immune system wavers in old age.

Her team has also discovered the presence of HSV-1 in the telltale plaques—clumps of proteins in the nerve cells of the brain—used to diagnose Alzheimer’s. In mice and cell cultures infected with HSV-1, they’ve found accumulation of two proteins, beta-amyloid and tau, that form the main components of, respectively, plaques and tangles—twisted protein fibers that form inside dying cells and are another defining characteristic of Alzheimer’s. Plaques and tangles, while sometimes found in normal aging brains, have been found to overflow in the brains of deceased Alzheimer’s sufferers; neuroscientists believe these protein accumulations can cause neuron death and tissue loss. Itzhaki speculates that herpes-infected cells may either produce the proteins in an attempt to fend off HSV-1 or, because the virus itself commands them to, the proteins somehow needed to jump-start the virus’s replication.

Itzhaki, Gale and their colleagues emphasize that rather than being the sole cause of memory loss, slower reaction time or depression, viral and bacterial infections are likely just one ingredient in a soup of risk factors. But for Alzheimer’s, HSV-1 could be especially significant. Itzhaki has found that elderly people who carried both HSV-1 in the brain and the e-4 subtype of the APOE gene (responsible for creating a protein that helps transport cholesterol throughout the body) were 12 times more likely to develop Alzheimer’s than people without either.

APOE-e4, already considered a significant risk factor for Alzheimer’s and thought to make us more vulnerable to viral infection, has also been linked to a greater risk of dementia in HIV-infected patients. In a 1997 Lancet paper, Itzhaki’s group concluded that HSV-1 infection, in conjunction with APOE-e4, could account for about 60 percent of the Alzheimer’s cases they studied. Due to limited funds, however, her group was able to study only a relatively low number of cases.

“I think the proposed theory is certainly reasonable given the supporting evidence,” says Iain Campbell, a professor of molecular biology at the University of Sydney. “What is difficult to establish here is actual causality.”

It might be the case that HSV-1 and other suspects aren’t responsible for the emergence of Alzheimer’s but are simply given free rein to worsen its symptoms as the neurodegenerative disorder weakens both the immune and nervous systems. Deciphering the relationship between these latent infections and Alzheimer’s will take more dedicated research, an effort that Itzhaki feels has been stymied by the persistent lack of resources available to her and her like-minded colleagues.

As things stand, though, she believes there is enough evidence to go ahead with treatment trials; for instance, giving Alzheimer’s patients HSV-1-targeted antivirals in hopes of slowing down or stopping the progression of the disease. She and a team of clinicians are trying to obtain a grant for such a pilot clinical trial to do just that.

Exasperated as Itzhaki has been, the headwinds against her and those who share her beliefs about the brain are slowly dying down. In some cases, once-derided and obscure scientists studying how infections affect the brain are now getting some financial support. There’s Jaroslav Flegr, for example, who has for decades theorized that T. gondii could alter human behavior and even cause certain forms of schizophrenia. In the wake of increased media attention, Flegr’s volume of work on T. gondii has noticeably stepped up as well. From 2014 to 2015, he co-authored 13 papers on T. gondii, nearly twice the number he published the previous two years; the trend of increased T. gondii papers holds across all of PubMed, the largest database of published biomedical research available. “ I have no serious problem with funding of my Toxo research now,” Flegr says.

As of now, though, there have been no ulcer-related Sherlock moments to prove a link between mental dysfunction and latent infections—only indirect correlations clumping together to form a blurry snapshot of a potential crime scene. Which is why Gale and others recommend a wait-and-see approach for the public, even as they acknowledge the potentially vast implications of their research. “I wouldn’t want someone to go out tomorrow and get a whole battery of tests,” he says. “There’s still a lot we need to understand.”

http://www.newsweek.com/viral-bacterial-links-brains-decline-462194

People who exercise at middle age might have bigger brains later on

On By A.P.In brain, exercise1 Comment

Poor physical fitness in middle age might be associated with a smaller brain size later on, according to a study published in an online issue of Neurology.

Brains shrink as people age, and the atrophy is related to cognitive decline and increased risk for dementia, a researcher said, and exercise reduces that deterioration and cognitive decline.

In this study, more than 1,500 people at an average age of 40 and without dementia or heart disease took a treadmill test. Twenty years later, they took another test, along with MRI brain scans. The study found those who didn’t perform as well on the treadmill test — a sign of poor fitness — had smaller brains 20 years later.

Among those who performed lower, people who hadn’t developed heart problems and weren’t using medication for blood pressure had the equivalent of one year of accelerated brain aging. Those who had developed heart problems or were using medication had the equivalent of two years of accelerated brain aging.

Their exercise capacity was measured using the length of time participants could exercise on the treadmill before their heart rate reached a certain level. Researchers measured heart rate and blood pressure responses to an early stage on the treadmill test, which provides a good picture for a person’s fitness level, according to the study author Nicole Spartano, a postdoctoral fellow at the Boston University School of Medicine.

Physical fitness is evolving as a significant factor related to cognitive health in older age. A study published in May 2015 found that higher levels of physical fitness in middle-aged adults were associated with larger brain volumes five years later.

This study shows that for people with heart disease, fitness might be particularly important for prevention of brain aging, Spartano said.

“We found that poor physical fitness in midlife was linked to more rapid brain aging two decades later,” she said. “This message may be especially important for people with heart disease or at risk for heart disease, in which we found an even stronger relationship between fitness and brain aging.”

The researchers also found that people with higher blood pressure and heart rate during exercise were more likely to have smaller brain sizes 20 years later. People with poor physical fitness usually have higher blood pressure and heart rate responses to low levels of exercise compared to people who exercise more, Spartano said

“From other studies, we know that exercise training programs that improve fitness may increase blood flow and oxygen to the brain over the short term,” Spartano said. “Over the course of a lifetime, improved blood flow may have an impact on brain aging and prevent cognitive decline in older age.”

The study suggests promotion of physical fitness during middle age is an important step toward ensuring healthy brain aging.

“The broad message,” Spartano said, “is that health and lifestyle choices that you make throughout your life may have consequences many years later.”

http://www.cnn.com/2016/02/15/health/poor-fitness-smaller-brain/index.html

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.

Scientists encode memories in a way that bypasses damaged brain tissue

On By A.P.In brain computer interface, brain-machine interface, neural prosthetics, neuroprosthetic device, Neuroscience, The Future, The SingularityLeave a comment

Researchers at University of South Carolina (USC) and Wake Forest Baptist Medical Center have developed a brain prosthesis that is designed to help individuals suffering from memory loss.

The prosthesis, which includes a small array of electrodes implanted into the brain, has performed well in laboratory testing in animals and is currently being evaluated in human patients.

Designed originally at USC and tested at Wake Forest Baptist, the device builds on decades of research by Ted Berger and relies on a new algorithm created by Dong Song, both of the USC Viterbi School of Engineering. The development also builds on more than a decade of collaboration with Sam Deadwyler and Robert Hampson of the Department of Physiology & Pharmacology of Wake Forest Baptist who have collected the neural data used to construct the models and algorithms.

When your brain receives the sensory input, it creates a memory in the form of a complex electrical signal that travels through multiple regions of the hippocampus, the memory center of the brain. At each region, the signal is re-encoded until it reaches the final region as a wholly different signal that is sent off for long-term storage.

If there’s damage at any region that prevents this translation, then there is the possibility that long-term memory will not be formed. That’s why an individual with hippocampal damage (for example, due to Alzheimer’s disease) can recall events from a long time ago – things that were already translated into long-term memories before the brain damage occurred – but have difficulty forming new long-term memories.

Song and Berger found a way to accurately mimic how a memory is translated from short-term memory into long-term memory, using data obtained by Deadwyler and Hampson, first from animals, and then from humans. Their prosthesis is designed to bypass a damaged hippocampal section and provide the next region with the correctly translated memory.

That’s despite the fact that there is currently no way of “reading” a memory just by looking at its electrical signal.

“It’s like being able to translate from Spanish to French without being able to understand either language,” Berger said.

Their research was presented at the 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society in Milan on August 27, 2015.

The effectiveness of the model was tested by the USC and Wake Forest Baptist teams. With the permission of patients who had electrodes implanted in their hippocampi to treat chronic seizures, Hampson and Deadwyler read the electrical signals created during memory formation at two regions of the hippocampus, then sent that information to Song and Berger to construct the model. The team then fed those signals into the model and read how the signals generated from the first region of the hippocampus were translated into signals generated by the second region of the hippocampus.

In hundreds of trials conducted with nine patients, the algorithm accurately predicted how the signals would be translated with about 90 percent accuracy.

“Being able to predict neural signals with the USC model suggests that it can be used to design a device to support or replace the function of a damaged part of the brain,” Hampson said.
Next, the team will attempt to send the translated signal back into the brain of a patient with damage at one of the regions in order to try to bypass the damage and enable the formation of an accurate long-term memory.

http://medicalxpress.com/news/2015-09-scientists-bypass-brain-re-encoding-memories.html#nRlv

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

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

New research suggests that memories may not be stored by synaptic connections between nerve cells

On By A.P.In Science, The Brain1 Comment

New research suggests that memories may not be stored by synaptic connections between neurons in the brain, but rather synapses may allow the expression of memories that are stored elsewhere in the neuron.

The revolutionary study by academics at the University of California has suggested for the first time that memories are not stored in synapses as previously thought. It is synapses, the connections between brain cells, that are destroyed by Alzheimer’s.

The breakthrough, reported in the highly regarded online journal eLife, could mean that it becomes possible to restore lost memories.

“Long-term memory is not stored at the synapse,” said David Glanzman, the study’s co-author and professor of integrative biology and physiology and of neurobiology at UCLA. “That’s a radical idea, but that’s where the evidence leads. The nervous system appears to be able to regenerate lost synaptic connections. If you can restore the synaptic connections, the memory will come back. It won’t be easy, but I believe it’s possible.”

Professor Glanzman’s team studied the marine snail Aplysia to understand the animal’s learning and memory functions. Glanzman was particularly interested in the Aplysia’s defensive reactions and the sensory and motor neurons responsible for its withdrawal response.

“If you train an animal on a task, inhibit its ability to produce proteins immediately after training, and then test it 24 hours later, the animal doesn’t remember the training,” said Prof. Glanzman. “However, if you train an animal, wait 24 hours, and then inject a protein synthesis inhibitor in its brain, the animal shows perfectly good memory 24 hours later. In other words, once memories are formed, if you temporarily disrupt protein synthesis, it doesn’t affect long-term memory. That’s true in the Aplysia and in human’s brains.”

As part of the test, the snails were given a number of electric shocks, which in themselves would not usually produce long-term memories. The team found that the memories they thought had been completely erased earlier in the experiment had returned, suggesting that synaptic connections that had previously been lost were apparently restored.

“That suggests that the memory is not in the synapses but somewhere else,” said Glanzman. “We think it’s in the nucleus of the neurons. We haven’t proved that, though.”

He added that the research could be a major breakthrough for Alzheimer’s sufferers as even though the disease destroys synapses in the brain, memories might not necessarily destroyed.

“As long as the neurons are still alive, the memory will still be there, which means you may be able to recover some of the lost memories in the early stages of Alzheimer’s,” said Prof Glanzman.

http://www.telegraph.co.uk/news/science/11307411/Cure-for-memory-loss-could-be-on-the-horizon.html