The Neuroscience Behind the Placebo Effect

by Viatcheslav Wlassoff, PhD | December 7, 2017 

As a child, did you ever feel better after your mother kissed your bumped knee? How do you think that worked? The power of suggestion—or the placebo effect—is a powerful psychological phenomenon that affects every aspect of our lives, dictating our preferences for food, drink, medication, social activities, and more.

Pioneering experiments describing the use of sham drugs date back to the late 18^th century. A version of John Quincy’s Lexicon Medicum published in 1811 defines the placebo as ‘an epithet given to any medicine adapted more to please than to benefit the patient’. However, physicians of the past tended to use forms of treatment that they assumed were ineffective, as opposed to the modern day usage of inert substances.

A wide variety of conditions have been proven to be amenable to placebos, including depression, sleep disorders, Parkinson’s disease, and pain². The placebo effect has been shown to impart tangible changes on the immune system similar to those who received real medication, where patients given syrup had increased white blood cell counts. Remarkably, patients with Parkinson’s disease stopped experiencing tremors and muscle stiffness after taking inert sugar pills. The success of mirror therapy in relieving phantom pain in amputees can be thought of as another example of the power of suggestion.

How our minds are fooled is not fully understood. The placebo effect may be an evolutionary adaptation that allows the brain to make quick decisions and assumptions about the environment. Consider this: if we had to analyse every single stimulus that our environment threws at us, we’d go mad in no time.

Scientists have identified that the psychological mechanisms of the placebo effect lie in both conscious expectations and learning. Although learning and expectations are not mutually exclusive, they are heavily dependent on each other.

To explain, when we expect a drug to reduce pain levels, our brains release endogenous endorphinsthat in turn are responsible for alleviating pain. On the other hand, the learning process involves integrating environmental and social cues in order to generate an internal expectation and subsequent placebo response. Experiencing repeated patterns of learning conditions (as in classical conditioning – think Pavlov’s dogs), causes a person to respond in a way that has spill-over-effects effects that influence unconscious physiological processes. 

Multiple studies have singled out the ventromedial prefrontal cortex (vmPFC) as a main player in mediating the placebo effect. Other areas of significant importance are the dorsolateral PFC, lateral orbitofrontal cortex, periaqueductal grey area, rostroventral medulla, and nucleus accumbens-ventral striatum.

In short, the complex underlying neuronal circuits involve the higher functioning areas of the brain (frontal cortices) and the seat of unconscious processes such as breathing, the brainstem. Interestingly, rsearch reports that the placebo effect is absent in those with Alzheimer’s disease (due to degeneration of the frontal cortex) and in patients subjected to external suppression of frontal cortex function via transcranial magnetic stimulation.

The endogenous opioid system and its role in placebo-induced analgesia is perhaps the best studied neurotransmitter system involved in the placebo effect. Naloxone, an opioid receptor antagonist, has been found to nullify the effects of placebo pain-killers. Other systems that have been implicated include the cannabinoid system.

These neuroanatomical and neurobiological findings likely have much room for growth and refinement considering that different placebo responses have been found to invoke different parts of the placebo circuit.

Given the complicated psychological mechanisms behind the placebo, it comes as no surprise that various factors are able to modulate its strength. Social context has a real impact on the placebo effect, as it fosters preconceived notions regarding treatment. For example, several trials showed that similar benefits were experienced by both groups of patients who underwent either traditional or sham Chinese acupuncture (the latter involving superficial needling at non-acupuncture points). The physician attitude and appearance of competency, as well as the cost, branding, shape, size, color, and taste of the pills were able to affect the perceived treatment efficacy.

It is common beleif that one must be unaware of the placebo in order for the placebo effect to work. Not so, argue a group of researchers from the University of Basel (Switzerland) and Harvard Medical School. They demonstrated that participants who were told that they were getting placebos and who received detailed explanations of the placebo effect experienced significant relief from heat-induced pain compared to those that were not told that they were given bogus drugs.

These surprising results underscore the formidable effects of the placebo effect and how much more there is still left to learn. Furthermore, this study opens doors to more ethically designed placebo-controlled studies. Withholding potentially beneficial treatment from patients in placebo-controlled trials is considered inherently unethical. However, with this study, it appears that full disclosure may not be that different to the traditional practices of keeping placebo patient groups in the dark.

In order to manipulate the placebo effect for clinical benefit, the notion of placebo responders and non-placebo responders was investigated. Are some people more amenable to the power of suggestion than others? If so, is it due to unchangeable genetic makeup or individual personality? Other questions that come to mind regard the persistency of the placebo effect. For how long does it last and does it transfer to other types of placebos? To illustrate, will a person responding to placebo painkillers for pain relief also respond to placebo antidepressants for improved moods?

In conclusion, we know that the placebo is a strong weapon in the clinician’s armamentarium. Despite that, the unpredictable variability of its effects obligates future research that enables us to get a better understanding of exactly when and for how long the placebo effect will work.

References: 

de craen A, Kaptchuk T, Tijssen J et al. Placebos and placebo effects in medicine: historical overview. J R Soc Med. 1999;92:511-515. PMCID: PMC1297390

Price DD, Finniss DG, Benedetti F. A comprehensive review of the placebo effect: recent advances and current thought. Annu. Rev. Psychol. 2008. 59:565–90. doi:10.1146/annurev.psych.59.113006.095941

Colloca L, Miller FG. How placebo responses are formed: a learning perspective. Philosophical Transactions of the Royal Society B: Biological Sciences. 2011;366(1572):1859-1869. doi:10.1098/rstb.2010.0398.

Geuter S, Koban L, Wager TD. The cognitive neuroscience of placebo effects: concepts, predictions and physiology. Annu. Rev. Neurosci. 2017. 40:167–88. doi:10.1146/annurev-neuro-072116-031132.

Wager TD, Atlas LY. The neuroscience of placebo effects: connecting context, learning and health. Nat Rev Neurosci. 2015 Jul;16(7):403-18. doi:10.1038/nrn3976.

Miller FG, Colloca L, Kaptchuk TJ. The placebo effect: illness and interpersonal healing. Perspectives in biology and medicine. 2009;52(4):518. doi:10.1353/pbm.0.0115.

Buckalew LW, Coffield KE. An investigation of drug expectancy as a function of capsule color and size and preparation form. J Clin Psychopharmacol. 1982 Aug;2(4):245-8. PMID: 7119132

Howe LC, Goyer, J. P., & Crum, A. J. Harnessing the placebo effect: Exploring the influence of physician characteristics on placebo response. Health Psychology. 2017;36(11):1074-82. doi:10.1037/hea0000499.

Locher C, Frey Nascimento A, Kirsch I et al. Is the rationale more important than deception? A randomized controlled trial of open-label placebo analgesia. Pain. 2017 Dec;158(12):2320-2328. doi:10.1097/j.pain.0000000000001012.

Image via frolicsomepl/Pixabay.

http://brainblogger.com/2017/12/07/the-neuroscience-behind-the-placebo-effect/

Meet the man who's walking 2,500 miles to fight Parkinson's disease

December 8, 2017    Donna Freydkin   TODAY

https://youtu.be/Of5XxJCLQh0

In the latest edition of People Helping People, our series celebrating acts of kindness, Megyn Kelly salutes Bill Bucklew, who’s walking 2,503 miles across America to raise money for the Michael J. Fox Foundation for Parkinson’s Research despite his own diagnosis of Parkinson’s at age 43.

https://www.today.com/health/meet-man-who-s-walking-2-500-miles-fight-parkinson-t119797

Many Different Types of Anxiety and Depression Exist

NEUROSCIENCE NEWS   DECEMBER 8, 2017
Source: Stanford.

Stanford researchers have identified five new categories of specific symptoms and brain area activations that can be applied to the diagnosis of anxiety and depression in a more specific manner.

Currently, depression and anxiety are the leading cause of disability and lost productivity worldwide with only one-third of patients recovering from treatment, the study said. NeuroscienceNews.com image is in the public domain.

Five new categories of mental illness that cut across the current more broad diagnoses of anxiety and depression have been identified by researchers in a Stanford-led study.

The five categories, defined by their specific symptoms and areas of brain activation, are: tension, anxious arousal, general anxiety, anhedonia — the inability to feel pleasure — and melancholia.

“We are trying to disentangle the symptom overlap in our current diagnoses which can ultimately guide tailored treatment choices,” the researchers wrote in their study, which was published in JAMA Psychiatry.

The research is part of an ongoing effort by Leanne Williams, PhD, professor of psychiatry and behavioral sciences and senior author of the study, and her lab, along with other groups within the field of psychiatric neuroscience, to better define mental illness in order to provide improved treatment plans for the millions of Americans who suffer from these disorders.

Currently, depression and anxiety are the leading cause of disability and lost productivity worldwide with only one-third of patients recovering from treatment, the study said.

The broad diagnostic categories as defined by the Diagnostic and Statistical Manual of Mental Disorders, such as anxiety and depression, have so many overlapping symptoms that it’s difficult to identify biological markers for potential treatments or cures, the researchers explained.

“Currently, the treatments would be the same for anyone in these broad categories,” Williams said. “By refining the diagnosis, better treatment options could be prescribed, specifically for that type of anxiety or depression.”

For their work, the researchers collected and processed data from 420 participants both with healthy diagnoses and with multiple anxiety and depression diagnoses. The participants underwent a series of tests involving brain mapping, self reporting of symptoms, and psychiatric diagnostic testing. Researchers measured how well participants functioned in everyday life, their capacity for building social relationships and general outlook on life.

The same tests were conducted with a second independent sample of 381 people. Using a data-driven approach that involved machine learning algorithms, researchers processed the data and were able to identify the same five new categories across both groups.

Results showed that 13 percent of participants were characterized by anxious arousal, 9 percent by general anxiety, 7 percent by anhedonia, 9 percent by melancholia and 19 percent by tension.

“Interestingly, we found that many people who did not meet diagnostic criteria, but were still experiencing some symptoms, fell into the tension type,” said Katherine Grisanzio, lead author of the study and research lab manager in Williams’ lab.

In the paper, the researchers further described the new categories:

• Tension: This type is defined by irritability. People are overly sensitive, touchy, and overwhelmed. The anxiety makes the nervous system hypersensitive.
• 
  
• Anxious arousal: Cognitive functioning, such as the ability to concentrate and control thoughts, is impaired. Physical symptoms include a racing heart, sweating, and feeling stressed. “People say things like ‘I feel like I’m losing my mind,” Williams said. “They can’t remember from one moment to the next.”
• 
  
• Melancholia: People experience problems with social functioning. Restricted social interactions further cause distress.
• 
  
• Anhedonia: The primary symptom is an inability to feel pleasure. This type of depression often goes unrecognized. People are often able to function reasonably well while in a high state of distress. “We see it in how the brain functions in overdrive,” Williams said. “People are able to power through but at some time become quite numb. These are some of the most distressed people.”
• 
  
• General anxiety: A generalized type of anxiety with the primary features involving worry and anxious arousal — a more physical type of stress.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Mark Michaud – Stanford

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Full open access research for “Transdiagnostic Symptom Clusters and Associations With Brain, Behavior, and Daily Function in Mood, Anxiety, and Trauma Disorders” by Katherine A. Grisanzio, BS; Andrea N. Goldstein-Piekarski, PhD; Michelle Yuyun Wang, BPsySc; Abdullah P. Rashed Ahmed, MS; Zoe Samara, PhD; Leanne M. Williams, PhD in JAMA Psychiatry. Published online December 3 2017 doi:10.1001/jamapsychiatry.2017.3951

Abstract

Transdiagnostic Symptom Clusters and Associations With Brain, Behavior, and Daily Function in Mood, Anxiety, and Trauma Disorders

Importance The symptoms that define mood, anxiety, and trauma disorders are highly overlapping across disorders and heterogeneous within disorders. It is unknown whether coherent subtypes exist that span multiple diagnoses and are expressed functionally (in underlying cognition and brain function) and clinically (in daily function). The identification of cohesive subtypes would help disentangle the symptom overlap in our current diagnoses and serve as a tool for tailoring treatment choices.

Objective To propose and demonstrate 1 approach for identifying subtypes within a transdiagnostic sample.

Design, Setting, and Participants This cross-sectional study analyzed data from the Brain Research and Integrative Neuroscience Network Foundation Database that had been collected at the University of Sydney and University of Adelaide between 2006 and 2010 and replicated at Stanford University between 2013 and 2017. The study included 420 individuals with a primary diagnosis of major depressive disorder (n = 100), panic disorder (n = 53), posttraumatic stress disorder (n = 47), or no disorder (healthy control participants) (n = 220). Data were analyzed between October 2016 and October 2017.

Main Outcomes and Measures We followed a data-driven approach to achieve the primary study outcome of identifying transdiagnostic subtypes. First, machine learning with a hierarchical clustering algorithm was implemented to classify participants based on self-reported negative mood, anxiety, and stress symptoms. Second, the robustness and generalizability of the subtypes were tested in an independent sample. Third, we assessed whether symptom subtypes were expressed at behavioral and physiological levels of functioning. Fourth, we evaluated the clinically meaningful differences in functional capacity of the subtypes. Findings were interpreted relative to a complementary diagnostic frame of reference.

Results Four hundred twenty participants with a mean (SD) age of 39.8 (14.1) years were included in the final analysis; 256 (61.0%) were female. We identified 6 distinct subtypes characterized by tension (n=81; 19%), anxious arousal (n=55; 13%), general anxiety (n=38; 9%), anhedonia (n=29; 7%), melancholia (n=37; 9%), and normative mood (n=180; 43%), and these subtypes were replicated in an independent sample. Subtypes were expressed through differences in cognitive control (F5,383 = 5.13, P < .001, ηp2 = 0.063), working memory (F5,401 = 3.29, P = .006, ηp2 = 0.039), electroencephalography-recorded β power in a resting paradigm (F5,357 = 3.84, P = .002, ηp2 = 0.051), electroencephalography-recorded β power in an emotional paradigm (F5,365 = 3.56, P = .004, ηp2 = 0.047), social functional capacity (F5,414 = 21.33, P < .001, ηp2 = 0.205), and emotional resilience (F5,376 = 15.10, P < .001, ηp2 = 0.171).

Conclusions and Relevance These findings offer a data-driven framework for identifying robust subtypes that signify specific, coherent, meaningful associations between symptoms, behavior, brain function, and observable real-world function, and that cut across DSM-IV-defined diagnoses of major depressive disorder, panic disorder, and posttraumatic stress disorder.

“Transdiagnostic Symptom Clusters and Associations With Brain, Behavior, and Daily Function in Mood, Anxiety, and Trauma Disorders” by Katherine A. Grisanzio, BS; Andrea N. Goldstein-Piekarski, PhD; Michelle Yuyun Wang, BPsySc; Abdullah P. Rashed Ahmed, MS; Zoe Samara, PhD; Leanne M. Williams, PhD in JAMA Psychiatry. Published online December 3 2017 doi:10.1001/jamapsychiatry.2017.3951

http://neurosciencenews.com/anxiety-depression-types-8138/

Population of Americans with Alzheimer’s Will More Than Double by 2060

NEUROSCIENCE NEWS  DECEMBER 8, 2017
Source: UCLA.

Researchers predict by 2060 around 15 million Americans will be living with MCI or Alzheimer’s disease. Currently, 6.08 million people are living with dementia.

The researchers examined the largest studies available on rates of progression of Alzheimer’s disease and used that information in a computer model they built that took into account the aging of the U.S population. The model projected the numbers of people in preclinical and clinical disease states. NeuroscienceNews.com image is in the public domain.

About 15 million Americans will have either Alzheimer’s dementia or mild cognitive impairment by 2060, up from approximately 6.08 million this year, according to a new study by researchers at the UCLA Fielding School of Public Health.

The findings highlight the need to develop measures that could slow the progression of the disease in people who have indications of neuropathological changes that could eventually lead to Alzheimer’s dementia, said Ron Brookmeyer, professor of biostatistics at the UCLA Fielding School of Public Health and the study’s lead author. The country’s population is aging and with it comes a growing number of people with Alzheimer’s disease.

The study was published today in the peer-reviewed Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association. The study is the first of its kind that has estimated the numbers of Americans with preclinical Alzheimer’s disease or mild cognitive impairment.

“There are about 47 million people in the U.S. today who have some evidence of preclinical Alzheimer’s, which means they have either a build-up of protein fragments called beta-amyloid or neurodegeneration of the brain but don’t yet have symptoms,” Brookmeyer said. “Many of them will not progress to Alzheimer’s dementia in their lifetimes. We need to have improved methods to identify which persons will progress to clinical symptoms, and develop interventions for them that could slow the progression of the disease, if not stop it all together.”

The researchers examined the largest studies available on rates of progression of Alzheimer’s disease and used that information in a computer model they built that took into account the aging of the U.S population. The model projected the numbers of people in preclinical and clinical disease states.

They found that by 2060 about 5.7 million Americans will have mild cognitive impairment and another 9.3 million will have dementia due to Alzheimer’s. Of the latter group, about 4 million Americans will need an intensive level of care similar to that provided by nursing homes. Mild cognitive impairment is an intermediate clinical stage that does not yet meet the threshold for dementia. Brookmeyer estimates that today about 2.4 million Americans are living with mild cognitive impairment due to Alzheimer’s disease.

“Estimates by disease state and severity are important because the resources needed to care for patients vary so much over the course of the illness,” Brookmeyer said.

There are some sources of uncertainty in the findings. Participants in the studies the researchers examined may not represent all demographics. Also, there are other types of dementia, such as vascular dementia, that were not examined but could have an impact on these numbers.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

The study’s co-authors are Nada Abdalla, a biostatistics doctoral student in the Fielding School, and Dr. Claudia Kawas and Maria Corrada of UC Irvine.

Funding: The National Institutes of Health (1R21AG055361) funded this study.

Source: Enrique Rivero – UCLA

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Abstract for “Forecasting the prevalence of preclinical and clinical Alzheimer’s disease in the United States” by Ron Brookmeyer, Nada Abdalla, Claudia H. Kawas, María M. Corrada in Alzheimer’s & Dementia. Published online December 6 2017 doi:10.1016/j.jalz.2017.10.009

Abstract

Forecasting the prevalence of preclinical and clinical Alzheimer’s disease in the United States

Introduction

We forecast the prevalence of preclinical and clinical Alzheimer’s disease (AD) and evaluated potential impacts of primary and secondary preventions in the United States.

Methods

We used a multistate model incorporating biomarkers for preclinical AD with US population projections.

Results

Approximately 6.08 million Americans had either clinical AD or mild cognitive impairment due to AD in 2017 and that will grow to 15.0 million by 2060. In 2017, 46.7 million Americans had preclinical AD (amyloidosis, neurodegeneration, or both), although many may not progress to clinical disease during their lifetimes. Primary and secondary preventions have differential impact on future disease burden.

Discussion

Because large numbers of persons are living with preclinical AD, our results underscore the need for secondary preventions for persons with existing AD brain pathology who are likely to develop clinical disease during their lifetimes as well as primary preventions for persons without preclinical disease.

“Forecasting the prevalence of preclinical and clinical Alzheimer’s disease in the United States” by Ron Brookmeyer, Nada Abdalla, Claudia H. Kawas, María M. Corrada in Alzheimer’s & Dementia. Published online December 6 2017 doi:10.1016/j.jalz.2017.10.009

http://neurosciencenews.com/alzheimers-population-2060-8130/

Canola Oil Linked to Worsened Memory and Learning Ability in Alzheimer’s

NEUROSCIENCE NEWS  DECEMBER 8, 2017
Source: Temple University Health System.

Temple University researchers report canola oil may have harmful effects on brain health. In a mouse model of Alzheimer’s disease, researchers discovered those exposed to canola oil in their diet had worsened memory and learning abilities.

Examination of brain tissue from the two groups of mice revealed that canola oil-treated animals had greatly reduced levels of amyloid beta 1-40. Amyloid beta 1-40 is the more soluble form of the amyloid beta proteins. It generally is considered to serve a beneficial role in the brain and acts as a buffer for the more harmful insoluble form, amyloid beta 1-42. NeuroscienceNews.com image is credited to Veganbaking.net.

Canola oil is one of the most widely consumed vegetable oils in the world, yet surprisingly little is known about its effects on health. Now, a new study published online December 7 in the journal Scientific Reports by researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) associates the consumption of canola oil in the diet with worsened memory, worsened learning ability and weight gain in mice which model Alzheimer’s disease. The study is the first to suggest that canola oil is more harmful than healthful for the brain.

“Canola oil is appealing because it is less expensive than other vegetable oils, and it is advertised as being healthy,” explained Domenico Praticò, MD, Professor in the Departments of Pharmacology and Microbiology and Director of the Alzheimer’s Center at LKSOM, as well as senior investigator on the study. “Very few studies, however, have examined that claim, especially in terms of the brain.”

Curious about how canola oil affects brain function, Dr. Praticò and Elisabetta Lauretti, a graduate student in Dr. Pratico’s laboratory at LKSOM and co-author on the new study, focused their work on memory impairment and the formation of amyloid plaques and neurofibrillary tangles in an Alzheimer’s disease mouse model. Amyloid plaques and phosphorylated tau, which is responsible for the formation of tau neurofibrillary tangles, contribute to neuronal dysfunction and degeneration and memory loss in Alzheimer’s disease. The animal model was designed to recapitulate Alzheimer’s in humans, progressing from an asymptomatic phase in early life to full-blown disease in aged animals.

Dr. Praticò and Lauretti had previously used the same mouse model in an investigation of olive oil, the results of which were published earlier in 2017.

In that study, they found that Alzheimer mice fed a diet enriched with extra-virgin olive oil had reduced levels of amyloid plaques and phosphorylated tau and experienced memory improvement. For their latest work, they wanted to determine whether canola oil is similarly beneficial for the brain.

The researchers started by dividing the mice into two groups at six months of age, before the animals developed signs of Alzheimer’s disease. One group was fed a normal diet, while the other was fed a diet supplemented with the equivalent of about two tablespoons of canola oil daily.

The researchers then assessed the animals at 12 months. One of the first differences observed was in body weight – animals on the canola oil-enriched diet weighed significantly more than mice on the regular diet. Maze tests to assess working memory, short-term memory, and learning ability uncovered additional differences. Most significantly, mice that had consumed canola oil over a period of six months suffered impairments in working memory.

Examination of brain tissue from the two groups of mice revealed that canola oil-treated animals had greatly reduced levels of amyloid beta 1-40. Amyloid beta 1-40 is the more soluble form of the amyloid beta proteins. It generally is considered to serve a beneficial role in the brain and acts as a buffer for the more harmful insoluble form, amyloid beta 1-42.

As a result of decreased amyloid beta 1-40, animals on the canola oil diet further showed increased formation of amyloid plaques in the brain, with neurons engulfed in amyloid beta 1-42. The damage was accompanied by a significant decrease in the number of contacts between neurons, indicative of extensive synapse injury. Synapses, the areas where neurons come into contact with one another, play a central role in memory formation and retrieval.

“Amyloid beta 1-40 neutralizes the actions of amyloid 1-42, which means that a decrease in 1-40, like the one observed in our study, leaves 1-42 unchecked,” Dr. Praticò explained. “In our model, this change in ratio resulted in considerable neuronal damage, decreased neural contacts, and memory impairment.”

The findings suggest that long-term consumption of canola oil is not beneficial to brain health. “Even though canola oil is a vegetable oil, we need to be careful before we say that it is healthy,” Dr. Praticò said. “Based on the evidence from this study, canola oil should not be thought of as being equivalent to oils with proven health benefits.”

The next step is to carry out a study of shorter duration to determine the minimum extent of exposure necessary to produce observable changes in the ratio of amyloid beta 1-42 to 1-40 in the brain and alter synapse connections. A longer study may be warranted in order to determine whether canola oil also eventually impacts tau phosphorylation, since no effects on tau were observed over the six-month exposure period.

“We also want to know whether the negative effects of canola oil are specific for Alzheimer’s disease,” Dr. Praticò added. “There is a chance that the consumption of canola oil could also affect the onset and course of other neurodegenerative diseases or other forms of dementia.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The research was funded in part by a grant from the Wanda Simone Endowment for Neuroscience.

Source: Jeremy Walter – Temple University Health System

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Veganbaking.net, licensed CC BY SA 2.0.

Original Research: Full open access research for “Effect of canola oil consumption on memory, synapse and neuropathology in the triple transgenic mouse model of Alzheimer’s disease” by Elisabetta Lauretti & Domenico Praticò in Scientific Reports. Published online December 7 2017 doi:10.1038/s41598-017-17373-3

Abstract

Effect of canola oil consumption on memory, synapse and neuropathology in the triple transgenic mouse model of Alzheimer’s disease

In recent years consumption of canola oil has increased due to lower cost compared with olive oil and the perception that it shares its health benefits. However, no data are available on the effect of canola oil intake on Alzheimer’s disease (AD) pathogenesis. Herein, we investigated the effect of chronic daily consumption of canola oil on the phenotype of a mouse model of AD that develops both plaques and tangles (3xTg). To this end mice received either regular chow or a chow diet supplemented with canola oil for 6 months. At this time point we found that chronic exposure to the canola-rich diet resulted in a significant increase in body weight and impairments in their working memory together with decrease levels of post-synaptic density protein-95, a marker of synaptic integrity, and an increase in the ratio of insoluble Aβ 42/40. No significant changes were observed in tau phosphorylation and neuroinflammation. Taken together, our findings do not support a beneficial effect of chronic canola oil consumption on two important aspects of AD pathophysiology which includes memory impairments as well as synaptic integrity. While more studies are needed, our data do not justify the current trend aimed at replacing olive oil with canola oil.

“Novel transcriptional networks regulated by CLOCK in human neurons” by Miles R. Fontenot, Stefano Berto, Yuxiang Liu, Gordon Werthmann, Connor Douglas, Noriyoshi Usui, Kelly Gleason, Carol A. Tamminga, Joseph S. Takahashi, and Genevieve Konopka in Genes & Development. Published online December 1 2017 doi:10.1101/gad.305813.117

Some Video Games Are Good For Older Adults’ Brains

NEUROSCIENCE NEWS   DECEMBER 6, 2017
Source: University of Montreal.

Using the classic Nintendo game, Super Mario 64, researchers discover playing 3D platform games could help older brains to stave off mild cognitive impairment. Researchers report older people who played the video game had gray matter increases in the cerebellum, hippocampus and dorsolateral prefrontal cortex.

The research team recruited 33 people, ages 55 to 75, who were randomly assigned to three separate groups. Participants were instructed to play Super Mario 64 for 30 minutes a day, five days a week, take piano lessons (for the first time in their life) with the same frequency and in the same sequence, or not perform any particular task. NeuroscienceNews.com image is in the public domain.

If you’re between 55 and 75 years old, you may want to try playing 3D platform games like Super Mario 64 to stave off mild cognitive impairment and perhaps even prevent Alzheimer’s disease.

That’s the finding of a new Canadian study by Université de Montréal psychology professors Gregory West, Sylvie Belleville and Isabelle Peretz. Published in PLOS ONE, it was done in cooperation with the Institut universitaire de gériatrie de Montréal (IUGM), Benjamin Rich Zendel of Memorial University in Newfoundland, and Véronique Bohbot of Montreal’s Douglas Hospital Research Centre.

In two separate studies, in 2014 and 2017, young adults in their twenties were asked to play 3D video games of logic and puzzles on platforms like Super Mario 64. Findings showed that the gray matter in their hippocampus increased after training.

The hippocampus is the region of the brain primarily associated with spatial and episodic memory, a key factor in long-term cognitive health. The gray matter it contains acts as a marker for neurological disorders that can occur over time, including mild cognitive impairment and Alzheimer’s.

West and his colleagues wanted to see if the results could be replicated among healthy seniors.

The research team recruited 33 people, ages 55 to 75, who were randomly assigned to three separate groups. Participants were instructed to play Super Mario 64 for 30 minutes a day, five days a week, take piano lessons (for the first time in their life) with the same frequency and in the same sequence, or not perform any particular task.

The experiment lasted six months and was conducted in the participants’ homes, where the consoles and pianos, provided by West’s team, were installed.

The researchers evaluated the effects of the experiment at the beginning and at the end of the exercise, six months later, using two different measurements: cognitive performance tests and magnetic resonance imaging (MRI) to measure variations in the volume of gray matter. This enabled them to observe brain activity and any changes in three areas:

• the dorsolateral prefrontal cortex that controls planning, decision-making and inhibition;
• the cerebellum that plays a major role in motor control and balance;
• and the hippocampus, the centre of spatial and episodic memory.

According to the MRI test results, only the participants in the video-game cohort saw increases in gray matter volume in the hippocampus and cerebellum. Their short-term memory also improved.

The tests also revealed gray matter increases in the dorsolateral prefrontal cortex and cerebellum of the participants who took piano lessons, whereas some degree of atrophy was noted in all three areas of the brain among those in the passive control group.

What mechanism triggers increases in gray matter, especially in the hippocampus, after playing video games? “3-D video games engage the hippocampus into creating a cognitive map, or a mental representation, of the virtual environment that the brain is exploring.,” said West. “Several studies suggest stimulation of the hippocampus increases both functional activity and gray matter within this region.”

Conversely, when the brain is not learning new things, gray matter atrophies as people age. “The good news is that we can reverse those effects and increase volume by learning something new, and games like Super Mario 64, which activate the hippocampus, seem to hold some potential in that respect,” said West. Added Belleville: “These findings can also be used to drive future research on Alzheimer’s, since there is a link between the volume of the hippocampus and the risk of developing the disease.”

“It remains to be seen,” concluded West, “whether it is specifically brain activity associated with spatial memory that affects plasticity, or whether it’s simply a matter of learning something new.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Jeff Heinrich – University of Montreal

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Full open access research for “Playing Super Mario 64 increases hippocampal grey matter in older adults” by Greg L. West, Benjamin Rich Zendel, Kyoko Konishi, Jessica Benady-Chorney, Veronique D. Bohbot, Isabelle Peretz, and Sylvie Belleville in PLOS ONE. Published online December 6 2017 doi:10.1371/journal.pone.0187779

Abstract

Playing Super Mario 64 increases hippocampal grey matter in older adults

Maintaining grey matter within the hippocampus is important for healthy cognition. Playing 3D-platform video games has previously been shown to promote grey matter in the hippocampus in younger adults. In the current study, we tested the impact of 3D-platform video game training (i.e., Super Mario 64) on grey matter in the hippocampus, cerebellum, and the dorsolateral prefrontal cortex (DLPFC) of older adults. Older adults who were 55 to 75 years of age were randomized into three groups. The video game experimental group (VID; n = 8) engaged in a 3D-platform video game training over a period of 6 months. Additionally, an active control group took a series of self-directed, computerized music (piano) lessons (MUS; n = 12), while a no-contact control group did not engage in any intervention (CON; n = 13). After training, a within-subject increase in grey matter within the hippocampus was significant only in the VID training group, replicating results observed in younger adults. Active control MUS training did, however, lead to a within-subject increase in the DLPFC, while both the VID and MUS training produced growth in the cerebellum. In contrast, the CON group displayed significant grey matter loss in the hippocampus, cerebellum and the DLPFC.

“Playing Super Mario 64 increases hippocampal grey matter in older adults” by Greg L. West, Benjamin Rich Zendel, Kyoko Konishi, Jessica Benady-Chorney, Veronique D. Bohbot, Isabelle Peretz, and Sylvie Belleville in PLOS ONE. Published online December 6 2017 doi:10.1371/journal.pone.0187779

http://neurosciencenews.com/aging-gaming-8125/