Category: Neurology

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Study Explores the Circadian Rhythm Control Centre

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Woman sleeping with an alarm clock on bedside. Photo by cottonbro from Pexels

Researchers in Japan have offered new insights into how the brain’s circadian rhythm control centre regulates behaviour.

Circadian rhythms are a force in the background that shapes many human behaviours such feeling tired and falling asleep, as well as influencing our health. Michihiro Mieda and his team at Kanazawa University in Japan are researching just how the brain’s circadian rhythm control centre regulates behaviour.

The control centre, known as the superchiasmatic nucleus, or SCN, contains many types of neurons that transmit signals using the molecule GABA, but little is known about how each type contributes to our bodily rhythms. In this most recent study, the researchers focused on GABA neurons that produce arginine vasopressin, a hormone that regulates kidney function and blood pressure in the body, and which the team recently showed is also involved in the regulation of the interval of rhythms produced by the SCN.

To examine the function of these neurons separate to all others, the researchers first deleted a gene in mice which was needed for GABA signaling between neurons, but only in vasopressin-producing SCN neurons. “We removed a gene that codes for a protein that allows GABA to be packaged before it is sent to other neurons,” explained Mieda. “Without packaging, none of the vasopressin neurons could send out any GABA signals.”

Thus, these neurons could not use GABA to communicate with the rest of the SCN anymore. The mice showed longer periods of activity, beginning activity earlier and ending activity later than control mice, a simple enough result. It might seem that losing the packaging gene in the neurons disrupted the molecular clock signal but the result was not so simple. Closer examination deepened the mystery as the molecular clock seemed to progress unhindered.
Using calcium imaging, the researchers examined the clock rhythms within the vasopressin neurons. They found that while the rhythm of activity matched the timing of behaviour in control mice, this relationship was disturbed in the mice with missing GABA transmission in the vasopressin neurons. The rhythm of SCN output, ie SCN neuronal electrical activity, in the modified mice had the same irregular rhythm as their behaviour.

“Our study shows that GABA signaling from vasopressin neurons in the suprachiasmatic nucleus help fix behavioral timing within the constraints of the molecular clock,” concluded Mieda.

Source: News-Medical.Net

Journal reference: Maejima, T., et al. (2021) GABA from vasopressin neurons regulates the time at which suprachiasmatic nucleus molecular clocks enable circadian behavior. PNAS. doi.org/10.1073/pnas.2010168118.

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Scientists Crack Neuron Information Storage Code

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A team of scientists from the UK and Australia have discovered that single neurons can store electrical patterns, similar to memories. This represents a breakthrough towards solving how neural systems are able to process and store information.

By comparing predictions from mathematical modeling to lab-based experiments with mammalian neurons, they were able to determine how different parameters, such as how long it takes for neuronal signals to be processed and how sensitive a cell is to external signals, affect how neural systems encode information.

The research team found that a single neuron is able to select between different patterns, dependent on the properties of each individual stimulus, for example slight differences in stimulation timing resulted in the emergence of no electrical activity spikes, single spikes per delay or two spikes per delay,

By opening up new avenues into research on the encoding of information in the brain and how this relates to memory formation, the study could also allow new insights into the causes and treatments of mental health conditions such as dementia.

“This work highlights how mathematical analysis and wet-lab experiments can be closely integrated to shed new light on fundamental problems in neuroscience,” said Dr Wedgwood. “That the theoretical predictions were so readily confirmed in experiments gives us great confidence in the mathematical approach as a tool for understanding how individual cells store patterns of activity. In the long run, we hope that this is the first step to a better understanding of memory formation in neural networks.”

Professor Krauskopf from the University of Auckland remarked, “The research shows that a living neuron coupled to itself is able to sustain different patterns in response to a stimulus. This is an exciting first step towards understanding how groups of neurons are able to respond to external stimuli in a precise temporal manner.”

“Communication between neurons occurs over large distances. The communication delay associated with this plays an important role in shaping the overall response of a network. This insight is crucial to how neural systems encode memories, which is one of the most fundamental questions in neuroscience,” added Professor Tsaneva from the University of Exeter’s Living Systems Institute.

Source: Medical Xpress

Journal information: Kyle C. A. Wedgwood et al, Robust spike timing in an excitable cell with delayed feedback, Journal of The Royal Society Interface (2021). dx.doi.org/10.1098/rsif.2021.0029

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Eye Pressure in Glaucoma not the Whole Story

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The findings of a new study in rats show that a chemical known to protect nerve cells also slows glaucoma, the leading cause of irreversible blindness.

According to the National Glaucoma Foundation, in the US, over 3 million have glaucoma, with only half being aware of the fact and more than 120 000 are blind from the disease. The World Health Organization estimates that, worldwide, over 60 million individuals suffer from glaucoma.  

Led by researchers at NYU Grossman School of Medicine, the study centred on the watery fluid inside the eye on which its function depends. In patients with glaucoma, a buildup of fluid pressure wears down cells in the eyes and the nerves connecting them to the brain.

Previous research that despite eye pressure having been controlled, the condition progressively worsened. The relationship between pressure buildup and impaired vision remains poorly understood

The new study showed that when rats ingested the compound citicoline, optic nerve signals between the brain and eye were almost fully restored. Citicoline is a major source of choline, a building block in the membranes that line nerve cells and enhance nerve cell communication. It is produced in the brain but also commercially produced.

The study confirmed that increased eye pressure levels contributes to nerve damage in glaucoma, but  it also showed that citicoline reduced vision loss in rats without reducing pressure levels.

“Our study suggests that citicoline protects against glaucoma through a mechanism different from that of standard treatments that reduce fluid pressure,” said senior author Kevin Chan, PhD, an assistant professor in the Department of Ophthalmology at NYU Langone Health. “Since glaucoma interrupts the connection between the brain and eye, we hope to strengthen it with new types of therapies.”

The findings are helping scientists better understand how glaucoma works and add to past evidence that citicoline may counter the disease, said Chan, also the director of the Neuroimaging and Visual Science Laboratory at NYU Langone. It is known that humans and rodents with glaucoma have lower than normal levels of choline in the brain, but until now, Prof Chan says, there’s been little concrete evidence of the effectiveness of choline supplements as a therapy for glaucoma or why choline occurs in lower levels in glaucoma patients.

Prof Chan and his team tested whether increasing levels of that chemical would slow or even stop the degradation of the optic nerve and other regions of the brain involved in vision. Using a comprehensive study of the eye-brain connection in glaucoma, his team found that giving rats oral doses of citicoline over a three-week period protected nerve tissues and reduced vision loss sustainably even after the treatment stopped for another three weeks.

To simulate glaucoma, the researchers used a clear gel in rats to build up eye pressure mildly without otherwise blocking their vision. Then, the team used MRI imagery to measure the structural integrity and the amount of functional and physiological activity along the visual pathway. To test the clarity of vision of each eye, the researchers tracked the rodents’ visual behaviour .

It was found that for rats with mildly elevated eye pressure, the tissues that connect the eye and brain, including the optic nerve, degraded for up to five weeks after the injury. Nerve structure breakdown in the citicoline-treated rodents slowed by up to 74%, which the researchers said indicates that the chemical had protective effects on nerve cells.

However, more research is necessary before citicoline supplements to treat glaucoma in humans, as commercial drugs have yet to be proven fully effective in clinical trials. The researchers are planning next to look into how choline protects the eye and why it is depleted in glaucoma patients.

Source: Medical Xpress

Journal information: Yolandi van der Merwe et al, Citicoline Modulates Glaucomatous Neurodegeneration Through Intraocular Pressure-Independent Control, Neurotherapeutics (2021). DOI: 10.1007/s13311-021-01033-6

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Impairment Lasts up to 10 Hours After Cannabis

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A comprehensive analysis of 80 scientific studies has identified a ‘window of impairment’ of between three and 10 hours caused by moderate to high doses of tetrahydrocannabinol (THC), the cannabis component that causes intoxication. According to the researchers, these results have consequences for drug-driving laws around the world.

How long the impairment lasts depends on the THC dose, whether it is taken orally or inhaled, on the usage habits of the cannabis user and the demands of the task. The psychoactive THC component of cannabis has potential medical applications in treating nausea, sleep apnoea, fibromyalgia and chronic pain, though these applications are controversial and currently difficult to study due to legal issues, though off-label use is common. 
Previous research by Dr Arkell and colleagues has shown that cannabidiol (CBD), one of the medically active components of cannabis, does not cause impairment in driving. CBD has analgesic and anti-inflammatory actions, as well as anxiolytic, antiemetic, antipsychotic, and neuroprotective antioxidant properties

Medical and non-medical legal cannabis use is on the rise worldwide.
THC causes acute impairment in driving and cognitive performance, but there is uncertainty among users about the duration of this impairment and when they can start tasks such as driving after consuming cannabis.
“Our analysis indicates that impairment may last up to 10 hours if high doses of THC are consumed orally,”  said lead author Dr Danielle McCartney, Lambert Initiative for Cannabinoid Therapeutics at the University of Sydney. “A more typical duration of impairment, however, is four hours, when lower doses of THC are consumed via smoking or vaporization and simpler tasks are undertaken (eg, those using cognitive skills such as reaction time, sustained attention and working memory). This impairment may extend up to six or seven hours if higher doses of THC are inhaled and complex tasks, such as driving, are assessed.”

A moderate THC dose is considered about 10 milligrams in this study, but could be higher for a regular user, said the researchers.

Co-author Dr Thomas Arkell, also from the Lambert Initiative, said: “We found that impairment is much more predictable in occasional cannabis users than regular cannabis users. Heavy users show significant tolerance to the effects of cannabis on driving and cognitive function, while typically displaying some impairment.”

Regular cannabis users might consume more to get the same effect, resulting in equivalent impairment, the authors noted.

In the case of oral use as in medical cannabis drops, tablets etc, the impairment takes longer to manifest and has a longer duration than the inhalation route.

The findings have implications for so-called drug-driving laws, the researchers said.

Professor Iain McGregor, Academic Director of the Lambert Initiative, said: “THC can be detected in the body weeks after cannabis consumption while it is clear that impairment lasts for a much shorter period of time. Our legal frameworks probably need to catch up with that and, as with alcohol, focus on the interval when users are more of a risk to themselves and others. Prosecution solely on the basis of the presence of THC in blood or saliva is manifestly unjust.

“Laws should be about safety on the roads, not arbitrary punishment. Given that cannabis is legal in an increasing number of jurisdictions, we need an evidence-based approach to drug-driving laws,” Prof McGregor said.

Source: News-Medical.Net

Journal information: McCartney, D., et al. (2021) Determining the magnitude and duration of acute Δ9-tetrahydrocannabinol (Δ9-THC)-induced driving and cognitive impairment: A systematic and meta-analytic review. Neuroscience & Biobehavioral Reviews. doi.org/10.1016/j.neubiorev.2021.01.003.

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Chronic Sinusitis Linked to Neural Functions

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A small proof-of-concept study found that sinonasal inflammation was associated with neural changes that could precede cognitive symptoms in young people.

In comparison to healthy controls, people with chronic rhinosinusitis showed decreased functional connectivity within the frontoparietal network, a major cognition modulating hub, in resting-state functional MRI imaging. The frontoparietal network allows individuals to coordinate behaviour in a rapid, accurate, and flexible goal-driven manner.

These individuals also had greater connectivity of this region to the default mode network (areas that are activated during introspective and self-referential processing) and decreased connectivity to the salience network (areas involved in detection and response to stimuli) on brain imaging, reported Aria Jafari, MD, of University of Washington in Seattle, and colleagues.

Compared to controls, individuals with more severe rhinosinusitis inflammation tended to have greater differences in functional connectivity, Dr Jafari and colleagues stated. 

“Although definitive conclusions are not possible given the limitations inherent in the data set, including lack of rhinosinusitis-specific clinical information, our results present initial evidence for functional connectivity alterations as a potential basis for cognitive impairments seen in patients affected by chronic rhinosinusitis and may help direct future research,” Dr Jafari and colleagues said.

However, in this study, no cognitive deficits accompanied the functional connectivity changes. People with chronic rhinosinusitis and their matched controls shared similar cognitive status and similar sleep quality, with no between-group differences in olfaction, taste, and pain, either.

It was suggested by the researchers that, “given the brain’s ability to adapt and compensate, particularly in young and cognitively healthy individuals, our findings may represent early and subclinical functional brain alterations that may precede or be more sensitive than anticipated behavioral responses.”

“It is possible that a clinical chronic rhinosinusitis cohort with broader age distribution and more significant symptoms may have even greater changes in functional brain connectivity in the regions identified in this study,” they added.

“Overall, I do think that this study gives credence to the large body of evidence that patients with chronic rhinosinusitis, or in this case sinonasal inflammation, do have issues with cognition,” commented Nicholas Rowan, MD, of Johns Hopkins University School of Medicine in Baltimore, who was not part of the study.

Sinonasal inflammation and chronic rhinosinusitis have well established negative impacts on quality of life, according to Rowan. Previous research has found that medical or surgical intervention for chronic rhinosinusitis can alleviate cognitive dysfunction.

“Though unfortunately, the findings here are not actionable from a clinical standpoint, they do provide novel information for further prospective study of patients with chronic rhinosinusitis, as well as laboratory studies that are aimed to better understand the mechanism of why patients with CRS have such substantial quality of life implications,” according to Dr Rowan.

Although comorbid psychiatric disorders and sleep dysfunction are among the proposed mechanisms for cognitive dysfunction, the researchers said their data was supportive of a direct association of immune molecules with brain function.

Using data from The Human Connectome Project, the case-control study included 22 people with radiologic sinonasal inflammation who were matched 1:1 by age and sex to healthy controls. Sinonasal inflammation was classified as moderate in 13 people and severe in nine.

All were young adults age 22 to 35, and 68% were male.

Limitations included the retrospective nature of the study and the small sample size. Since cognitively normal participants identified radiographically from a large database, this limited the generalisability of the results, the authors added.

“Future prospective studies are warranted to determine the applicability of these findings to a clinical chronic rhinosinusitis population,” they said.

Source: MedPage Today

Journal information: Jafari A, et al “Association of sinonasal inflammation with functional brain connectivity” JAMA Otolaryngal Head Neck Surg 2021; DOI: 10.1001/jamaoto.2021.0204.

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Brain Glue Heals Neural Damage from Brain Injuries

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In a new study, researchers at the University of Georgia’s (UGA) Regenerative Biosciences Center have shown that the “brain glue” they developed protects against loss of brain tissue after a severe injury, and may also help in functional neural repair.

Significant traumatic brain injury (TBI) commonly results in extensive tissue loss and long-term disability, with no clinical treatments available to prevent this.

The new finding is the first to provide visual and functional evidence of the repair of brain neural circuits involved in reach-to-grasp movement in brain glue-implanted animals following severe TBI.

“Our work provides a holistic view of what’s going on in the recovery of the damaged region while the animal is accomplishing a specific reach-and-grasp task,” said lead investigator Lohitash Karumbaiah, an associate professor in the University of Georgia’s College of Agricultural and Environmental Sciences.

The brain glue developed by Prof Karumbaiah was designed to mimic the meshwork of sugars supporting brain cells. The hydrogel contains key structures that bind to two protective protein factors that can enhance the survival and regrowth of brain cells after severe TBI: basic fibroblast growth factor and brain-derived neurotrophic factor.

In previous research, Prof Karumbaiah and his team demonstrated that the brain glue conferred significant protection to brain tissue from severe TBI damage. In order to tap the neuroprotective capability of the original, they changed the delivery surface of protective factors to help accelerate the regeneration and functional activity of brain cells.

“Animal subjects that were implanted with the brain glue actually showed repair of severely damaged tissue of the brain,” said Karumbaiah. “The animals also elicited a quicker recovery time compared to subjects without these materials.”

The team used a tissue-cleaning method to make the brain less opaque, allowing them to 3-D image the cells’ response in the reach-to-grasp circuit, which is similar in rats and humans.

“Because of the tissue-clearing method, we were able to obtain a deeper view of the complex circuitry and recovery supported by brain glue,” said Prof Karumbaiah. “Using these methods along with conventional electrophysiological recordings, we were able to validate that brain glue supported the regeneration of functional neurons in the lesion cavity.”

“Doing the behavioral studies, the animal work and the molecular work sometimes takes a village,” said Karumbaiah. “This research involved a whole cross-section of RBC undergraduate and graduate students, as well as faculty members from both UGA and Duke University.”

Source: Medical Xpress

Journal information: Charles-Francois V. Latchoumane et al. Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury, Science Advances (2021). DOI: 10.1126/sciadv.abe0207

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Study Reveals More Secrets of Leptin’s Role in Appetite Control

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A new study describes how leptin, an appetite-suppressing hormone released from adipose tissue, is involved in appetite suppression through the dopamine pathway.  

Since the discovery of leptin in the 1990s, many questions still remain over how it suppresses appetite. Now, a new study in mice describes novel neurocircuitry between midbrain structures that control feeding behaviours under the modulatory control of leptin.

Leptin links the body and the brain, providing information about its metabolic state and influencing energy balance. Animals deficient for leptin rapidly become obese without its regulatory control of feeding behaviour, showing just how important it is.

“This process is shaped by communication between bodily fat storages (via a hormone called leptin) and the brain’s dopamine reward system. This leptin-dopamine axis is critically important for body weight control, but its modes of action were not well understood,” said Roger Adan, PhD, Department of Translational Neuroscience, University Medical Centre Utrecht.

Not only does leptin suppress eating through signals to brain regions controlling eating behaviours, but it also lowers food’s reward value in the brain’s dopamine (DA) reward system. That food-reward pathway was known to involve dopaminergic neurons of the ventral tegmental area (VTA) signaling to the nucleus accumbens (NAc). However, these DA neurons do not have receptors for leptin.

The researchers mapped the new microcircuitry with a combination of technologies, including optogenetics, chemogenetics and electrophysiology.

“Although leptin receptors are present on [some] dopamine neurons that signal food reward, we discovered that leptin receptors are also present on inhibitory neurons that more strongly regulate the activity of dopamine neurons. Some of these inhibitory neurons suppressed food seeking when [animals were] hungry, whereas others [did so] only when [animals were] in a sated state,” said Professor Adan, also of the Department of Translational Neuroscience, University Medical Center Utrecht and University Utrecht.

John Krystal, MD, Editor of Biological Psychiatry, said of the study, “It turns out that leptin plays key modulatory roles in an elegant circuit that unites midbrain and limbic reward circuitry. By inhibiting hypothalamic neurons and ultimately suppressing the activity of dopamine neurons in the midbrain that signal reward and promote feeding, leptin reduces food intake in animals under conditions when caloric intake has exceeded energy use.”

Professor Adan concluded that, “Targeting these neurons may provide a new avenue for the treatment of anorexia nervosa and to support dieting in people with obesity.”

Source: News-Medical.Net

Journal information: Omrani, A., et al. (2021) Identification of novel neurocircuitry through which leptin targets multiple inputs to the dopamine system to reduce food reward seeking. Biological Psychiatry. doi.org/10.1016/j.biopsych.2021.02.017.

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Shared Neural System May Be Used for Different Memory Stores

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The brain may have a shared neural system that is involved in the retrieval of facts and personal memories used in everyday life, new research has found.

Factual memory had long been categorised into two stores; factual memory and memory of personal experiences. These two repositories in concert enable people to make sense of the world around them. Individuals with retrograde amnesia can fail to remember personal experiences, but still recall factual knowledge. These two stores have been shown by decades of clinical and experimental research to be stored across two separate regions of the brain.

But the new study suggests that a shared set of brain regions play an important role in controlling the successful retrieval of weak memories.

When participants were asked to retrieve fact memories and personal memories, researchers used functional MRI imaging to study how these regions changed in activity levels.

Lead researcher Dr Deniz Vatansever, formerly of the University of York and now working for the Institute of Science and Technology for Brain-inspired Intelligence, Fudan University said: “The new research suggests that despite their functional differences, successfully retrieving weak information from these two memory systems might be dependent upon a shared brain mechanism.

“Our memories allow us to make sense and flexibly interact with the world around us. Although in most cases, our strongly encoded memories might be sufficient for the task at hand, remembering to pack a beach towel for an upcoming seaside holiday, this strong memory may be irrelevant in other instances, such as when packing for a business trip. As such, we need to tightly control the retrieval of relevant memories to solve different tasks under different circumstances. Our results indicate that this control process might be shared across both factual and personal memory types.”

The researchers said their findings may be applicable to memory disorders, including dementia, where patients’ quality of life is affected by being unable to remember important information. The findings could also be relevant in the development of a new generation of AI, which use long-term memory in solving computational problems. 

“In order to generate appropriate thoughts and behaviors, we have to draw on our memory stores in a highly flexible way,” said senior author Elizabeth Jefferies, and professor, Department of Psychology, University of York. “This new study highlights control processes within the brain that allow us to focus on unusual aspects of the meanings of words and to retrieve weakly encoded personal experiences. This control over memory allows us to be creative and to adapt as our goals or circumstances change.”

Source: News-Medical.Net

Journal information: Vatansever, D., et al. (2021) Varying demands for cognitive control reveals shared neural processes supporting semantic and episodic memory retrieval. Nature Communications. doi.org/10.1038/s41467-021-22443-2.

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Sugar-sweetened Drinks During Adolescence Impacts Cognition in Adulthood

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New research has shown that, in rats, daily consumption of sugar-sweetened drinks during adolescence impairs performance on a learning and memory task during adulthood. 

The researchers also demonstrated that changes in the bacteria in the gut may be the key to the sugar-induced memory impairment. Evidence in support of this comes from the observation of similar memory deficits even when the bacteria, called Parabacteroides, were experimentally enriched in the guts of animals that had never consumed sugar.

“Early life sugar increased Parabacteroides levels, and the higher the levels of Parabacteroides, the worse the animals did in the task,” said first author Emily Noble, assistant professor, College of Family and Consumer Sciences, University of Georgia. “We found that the bacteria alone was sufficient to impair memory in the same way as sugar, but it also impaired other types of memory functions as well.”

Data from the Centers for Disease Control and Prevention show American children between the ages 9-18 exceed the recommendation of limiting added sugars to less than 10 percent of calories per day, with the bulk of the calories coming from sugar-sweetened beverages.

Since the hippocampus is still developing into late adolescence and plays a role in a variety of cognitive functions, researchers sought to understand more about its susceptibility to a high-sugar diet via gut microbiota.

Juvenile rats were given their normal chow and an 11% sugar solution, comparable to commercially available sugar-sweetened beverages. Researchers then had the rats perform a hippocampus-dependent memory task designed to measure episodic contextual memory, or remembering the context where they had seen a familiar object before.

“We found that rats that consumed sugar in early life had an impaired capacity to discriminate that an object was novel to a specific context, a task the rats that were not given sugar were able to do,” Prof Noble said.

A second memory task measured basic recognition memory, a hippocampal-independent memory function that involves the animals’ ability to recognise something they had seen previously. Sugar had no effect on the animals’ recognition memory.

“Early life sugar consumption seems to selectively impair their hippocampal learning and memory,” Prof Noble said.

Further analysis revealed that high sugar consumption led to elevated levels of Parabacteroides in the gut microbiome, the more than 100 trillion microorganisms in the gastrointestinal tract that play a role in human health and disease.

To determine the mechanism by which bacteria impacted memory and learning, researchers experimentally increased levels of Parabacteroides in the microbiome of rats that had never consumed sugar. Those animals showed impairments in both hippocampal dependent and hippocampal-independent memory tasks.

“(The bacteria) induced some cognitive deficits on its own,” Prof Noble said.

Future research is needed to better identify these gut-brain signaling specific pathways.

“The question now is how do these populations of bacteria in the gut alter the development of the brain?” Prof Noble said. “Identifying how the bacteria in the gut are impacting brain development will tell us about what sort of internal environment the brain needs in order to grow in a healthy way.”

Source: News-Medical.Net

Journal information: Noble, E. E., et al. (2021) Gut microbial taxa elevated by dietary sugar disrupt memory function. Translational Psychiatry. doi.org/10.1038/s41398-021-01309-7.

Categories : Diseases, Syndromes and Conditions NeurologyTags :

Mystery Brain Disease Baffles Canadian Doctors

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Doctors in Canada are struggling to explain a spate of cases involving memory loss, hallucinations and muscle atrophy.

For more than a year public health officials in New Brunswick province have been tracking a “cluster” of 43 cases of suspected neurological disease with no known cause.

A leaked memo from the province’s public health agency asking physicians to be on the lookout for symptoms similar to Creutzfeldt-Jakob disease (CJD), a rare, fatal and largely sporadic disease caused by prion proteins. Symptoms such as memory loss, vision problems and abnormal jerking movements were similar enough to trigger an alert with Canada’s CJD surveillance network. However, it was confirmed that this disease was not CJD.

“We don’t have evidence to suggest it’s a prion disease,” said Dr Alier Marrero, the neurologist leading New Brunswick’s investigation.
Patients initially reported unexplained pains, spasms and behavioural changes, easily misdiagnosed as anxiety or depression.

However, over 18 to 36 months they began to develop cognitive decline, muscle wasting, drooling and teeth chattering. Some also began experiencing frightening hallucinations, including the sensation of crawling insects on their skin.  

Each time a possible case arises, a battery of tests is administered to determine if they match the cluster. Cases have risen from only one in 2015 to 24 in 2020, and so far five people are believed to have died from the illness.

“We have not seen over the last 20-plus years a cluster of diagnosis-resistant neurological disease like this one,” said Michael Coulthart, head of Canada’s CJD surveillance network.

The majority of cases are linked a sparsely populated region of the province, with the overall number of cases in the cluster remaining low. However, New Brunswick has a population of fewer than 800 000 people.

Dr Marrero and his team have consulted experts in neurology, environmental health, field epidemiology, zoonotics and toxicology to better understand the possible cause of the mysterious illness.

A growing team of researchers are trying to pin down a common cause or perhaps environmental effect.

“We don’t know what is causing it,” said Dr Marrero. “At this time we only have more patients appearing to have this syndrome.”

Valerie Sim, a researcher of neurodegenerative diseases at the University of Alberta cautioned against jumping to conclusions. “I don’t really know if we even have a defined syndrome. There just isn’t enough information yet,” she said.

She observed that key markers for degenerative neurological illnesses had not been identified, with the cluster’s wide range of symptoms being “atypical” for most brain diseases. Conversely, the scope of symptoms could be explained by certain cancers, dementia or even misdiagnoses.

Frustratingly, when the ailment is unclear a number of tools can be deployed, “and then the patient somehow recovers. You come away never knowing what they actually had,” said Sim.

“We see odd neurological syndromes from time to time. Sometimes we figure them out. Sometimes we don’t.”

Source: The Guardian