Posts Tagged ‘cognitive decline’

A team from the Department of Psychological Medicine and Department of Biochemistry at the Yong Loo Lin School of Medicine at the National University of Singapore (NUS) has found that seniors who consume more than two standard portions of mushrooms weekly may have 50 per cent reduced odds of having mild cognitive impairment (MCI).

A portion was defined as three quarters of a cup of cooked mushrooms with an average weight of around 150 grams. Two portions would be equivalent to approximately half a plate. While the portion sizes act as a guideline, it was shown that even one small portion of mushrooms a week may still be beneficial to reduce chances of MCI.

“This correlation is surprising and encouraging. It seems that a commonly available single ingredient could have a dramatic effect on cognitive decline,” said Assistant Professor Lei Feng, who is from the NUS Department of Psychological Medicine, and the lead author of this work.

The six-year study, which was conducted from 2011 to 2017, collected data from more than 600 Chinese seniors over the age of 60 living in Singapore. The research was carried out with support from the Life Sciences Institute and the Mind Science Centre at NUS, as well as the Singapore Ministry of Health’s National Medical Research Council. The results were published online in the Journal of Alzheimer’s Disease on 12 March 2019.

Determining MCI in seniors

MCI is typically viewed as the stage between the cognitive decline of normal ageing and the more serious decline of dementia. Seniors afflicted with MCI often display some form of memory loss or forgetfulness and may also show deficit on other cognitive function such as language, attention and visuospatial abilities. However, the changes can be subtle, as they do not experience disabling cognitive deficits that affect everyday life activities, which is characteristic of Alzheimer’s and other forms of dementia.

“People with MCI are still able to carry out their normal daily activities. So, what we had to determine in this study is whether these seniors had poorer performance on standard neuropsychologist tests than other people of the same age and education background,” explained Asst Prof Feng. “Neuropsychological tests are specifically designed tasks that can measure various aspects of a person’s cognitive abilities. In fact, some of the tests we used in this study are adopted from commonly used IQ test battery, the Wechsler Adult Intelligence Scale (WAIS).”

As such, the researchers conducted extensive interviews and tests with the senior citizens to determine an accurate diagnosis. “The interview takes into account demographic information, medical history, psychological factors, and dietary habits. A nurse will measure blood pressure, weight, height, handgrip, and walking speed. They will also do a simple screen test on cognition, depression, anxiety,” said Asst Prof Feng.

After this, a two-hour standard neuropsychological assessment was performed, along with a dementia rating. The overall results of these tests were discussed in depth with expert psychiatrists involved in the study to get a diagnostic consensus.

Mushrooms and cognitive impairment

Six commonly consumed mushrooms in Singapore were referenced in the study. They were golden, oyster, shiitake and white button mushrooms, as well as dried and canned mushrooms. However, it is likely that other mushrooms not referenced would also have beneficial effects.

The researchers believe the reason for the reduced prevalence of MCI in mushroom eaters may be down to a specific compound found in almost all varieties. “We’re very interested in a compound called ergothioneine (ET),” said Dr. Irwin Cheah, Senior Research Fellow at the NUS Department of Biochemistry. “ET is a unique antioxidant and anti-inflammatory which humans are unable to synthesise on their own. But it can be obtained from dietary sources, one of the main ones being mushrooms.”

An earlier study by the team on elderly Singaporeans revealed that plasma levels of ET in participants with MCI were significantly lower than age-matched healthy individuals. The work, which was published in the journal Biochemical and Biophysical Research Communications in 2016, led to the belief that a deficiency in ET may be a risk factor for neurodegeneration, and increasing ET intake through mushroom consumption might possibly promote cognitive health.

Other compounds contained within mushrooms may also be advantageous for decreasing the risk of cognitive decline. Certain hericenones, erinacines, scabronines and dictyophorines may promote the synthesis of nerve growth factors. Bioactive compounds in mushrooms may also protect the brain from neurodegeneration by inhibiting production of beta amyloid and phosphorylated tau, and acetylcholinesterase.

Next steps

The potential next stage of research for the team is to perform a randomised controlled trial with the pure compound of ET and other plant-based ingredients, such as L-theanine and catechins from tea leaves, to determine the efficacy of such phytonutrients in delaying cognitive decline. Such interventional studies will lead to more robust conclusion on causal relationship. In addition, Asst Prof Feng and his team also hope to identify other dietary factors that could be associated with healthy brain ageing and reduced risk of age-related conditions in the future.

https://medicalxpress.com/news/2019-03-mushrooms-cognitive-decline.html

brains-immune-cells-to-blame-for-obesity-associated-cognitive-decline-309339

Obesity leads to cognitive impairment by activating microglial cells, which consume otherwise functional synapses in the hippocampus, according to a study of male mice published in JNeurosci. The research suggests that microglia may be a potential therapeutic target for one of the lesser known effects of this global health epidemic on the brain.

Nearly two billion adults worldwide are overweight, more than 600 million of whom are obese. In addition to increasing risk of conditions such as diabetes and heart disease, obesity is also a known risk factor for cognitive disorders including Alzheimer’s disease. The cellular mechanisms that contribute to cognitive decline in obesity, however, are not well understood.

Elise Cope and colleagues replicated previous research by demonstrating diet-induced obesity in mice impairs performance on cognitive tasks dependent on the hippocampus and results in loss of dendritic spines — the neuronal protrusions that receive signals from other cells — and activates microglia. Using genetic and pharmacological approaches to block microglial activity, the researchers established microglia are causally linked to obesity-induced dendritic spine loss and cognitive decline. The results suggest obesity may drive microglia into a synapse-eating frenzy that contributes to the cognitive deficits observed in this condition.

https://www.technologynetworks.com/neuroscience/news/brains-immune-cells-to-blame-for-obesity-associated-cognitive-decline-309339?utm_campaign=NEWSLETTER_TN_Neuroscience_2017&utm_source=hs_email&utm_medium=email&utm_content=65859986&_hsenc=p2ANqtz-8GahP4LE2EOoHR4ShLvP0WjIDGrQksSkIDt93_VTrGea3qFC8v7VaOr9RXxmjjl8VDuNn2DK1PVOXEa5FBOdgl-GvhlA&_hsmi=65859986

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

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.

http://mobile.nytimes.com/2015/03/21/business/alzheimers-drug-trial-shows-cognitive-decline-sharply-slowed.html?referrer=&_r=0