Category: Neurology

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Study Uncovers a Key Brain Building Block

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Astrocytes (red) from a rat brain. Credit: Jeffrey C. Smith Lab, National Institute of Neurological Disorders and Stroke, NIH

A new study from Duke and UNC scientists has discovered a crucial protein involved in the communication and coordination between astrocytes as they build synapses — essentially a brain building block. 

Astrocytes, specialised, star-shaped glial cells that outnumber the neurons they support over fivefold and which make up about half the mass of a human brain, are increasingly being viewed as having a critical role in shaping the development of the brain.  Astrocytes tile the entire central nervous system (CNS) and exert many essential complex functions in the healthy CNS, including guiding development of the brain. 

The researchers found that a molecule, called hepaCAM, is a key component of this process. Without it, astrocytes aren’t as sticky as they should be, and tend to stick to themselves rather than forming connections with their neighbouring astrocytes.

This finding, in studies on mice with the gene for hepaCAM deleted from their astrocytes, helps in the understanding of several brain disorders, including cognitive decline, epilepsy and autism spectrum disorders.

One rare brain disorder, called megalencephalic leukoencephalopathy (MLC) is also known to be caused by a mutation in the hepaCAM gene, and this work might provide answers about what exactly has gone wrong. MLC is a developmental disorder that grows progressively worse, causing macrocephaly (a large head), swelling of the brain’s white matter, intellectual disability and epilepsy.

By deleting hepaCAM from astrocytes to see what it does, “we sort of made the cells into introverts,” explained senior author Cagla Eroglu, an associate professor of cell biology at the Duke University School of Medicine. “They’re normally wanting to reach out, but without hepaCAM, they started to hug themselves instead.”

“If the astrocyte makes junctions to its neighbours, then you start to have a network,” Prof Eroglu said. “To make a functional brain, you need a functional astrocytic network.”

The researchers zeroed in on hepaCAM by searching for highly active genes in astrocytes, and which have been implicated in brain dysfunction. They partnered with another group working on hepaCAM at the University of Barcelona, but that group has been  looking at the molecule for its role in regulating chloride signaling channels in astrocytes.

The Duke group found that deleting hepaCAM from astrocytes led to a synaptic network that was too easily excited and not as well dampened. “The effect on the inhibitory synapses was the strongest,” said first author Katie Baldwin, who recently became an assistant professor of cell biology and physiology at the University of North Carolina at Chapel Hill. “You’re putting the inhibition down and the excitation up, so that really could point to a mechanism for epilepsy.”

Prof Baldwin plans to test whether hepaCAM-deficient mice have behavioural differences or changes in learning and memory, or whether they exhibit the stress and social anxiety that are markers of autism spectrum disorders. She said they might also reintroduce the disease-mutation versions of the protein to mice that were born without it to see what effects it has.

“We know hepaCAM is interacting with itself between two astrocytes, but we don’t know what it’s interacting with at the synapse,” Prof Baldwin said. “We don’t know if it could be interacting with hepaCAM which is also found in the neurons, or if it could be some other protein that we don’t know about yet.

Source: Duke University School of Nursing

Journal information: Katherine T. Baldwin et al, HepaCAM controls astrocyte self-organization and coupling, Neuron (2021). DOI: 10.1016/j.neuron.2021.05.025

Categories : Cardiovascular Disease NeurologyTags :

Statins not Associated With Cognitive Decline

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A new study has found that statin use in adults 65 years old or older is not associated with incident dementia, mild cognitive impairment (MCI) or decline in individual cognition domains.

Major health concerns in the elderly, cognitive decline and dementia affect about 10% of people over 60 years old. Statins are used to reduce low-density lipoprotein cholesterol, and are a fundamental treatment for prevention of primary and secondary cardiovascular disease (CVD) events. 
In 2012 the Food and Drug Administration issued a warning about cases of apparent short-term cognitive impairment with statin use, while acknowledging that the cardiovascular benefits outweigh their risks. Systematic reviews have since shown insufficient evidence on the impact of statins, and research has shown mixed results, with some showing a neurocognitive benefit of statins and others reporting a null effect.

“With statins being increasingly prescribed to older adults, their potential long-term effects on cognitive decline and dementia risk have attracted growing interest,” said lead author Zhen Zhou, PhD, Menzies Institute for Medical Research at the University of Tasmania. “The present study adds to previous research by suggesting that statin use at baseline was not associated with subsequent dementia incidence and long-term cognitive decline in older adults.”

Researchers of this study analysed data from the ASPirin in Reducing Events in the Elderly (ASPREE) trial. ASPREE was a large prospective, randomized placebo-controlled trial of daily low-dose aspirin with adults 65 or older. One of the key selection criteria of ASPREE was that participants had to have a score of 78 for the Modified Mini-Mental State Examination test, a screening test for cognitive abilities, at enrollment.

The study had 18 846 participants, grouped by their baseline statin use (31.3% of participants) versus non-statin use. The study aimed to measure outcomes including incident dementia and its subclassifications (probable Alzheimer’s disease [AD], mixed presentations); MCI and its subclassifications (MCI consistent with AD, MCI-other); changes in domain-specific cognition including global cognition, memory, language and executive function, and psychomotor speed; and in the composite of these domains.

After a median of 4.7 years of follow-up, researchers found 566 incident cases of dementia (including probable AD and mixed presentations). Compared with no statin use, statin use was not associated with risk of all-cause dementia, probable AD or mixed presentations of dementia. There were 380 incident cases of MCI found (including MCI consistent with AD and MCI-other). Compared to no statin use, statin use was not associated with risk of MCI, MCI consistent with AD or other MCI. No statistically significant difference in the change of composite cognition and any individual cognitive domains between statin users versus non-statin users was seen. However, researchers did find interaction effects between baseline cognitive ability and statin therapy for all dementia outcomes.

The researchers acknowledged several limitations, including observational study bias and lack of data on the length of prior use of statins; and the dose of statins was not recorded in the ASPREE trial, so their effects could not be fully explored. Researchers conclude the study must be interpreted with caution and will require confirmation by randomized clinical trials designed to explore the neurocognitive effects of statins in older populations.

In an accompanying editorial comment, Christie M. Ballantyne, MD, professor at Baylor College of Medicine in Houston, noted study limitations that the authors address, but agreed the findings suggest statins do not contribute to cognitive decline.

“Overall, the analysis was well done, and its main strengths are a large cohort with a battery of standardised tests that allowed the investigators to track both cognition and incidence of dementia and its subtypes over time,” Ballantyne said. “Lingering questions such as the one raised by this analysis regarding potential adverse effects of statins in individuals with mildly impaired cognition can only be answered in randomised controlled trials in the appropriate age group and population and with appropriate testing and adequate follow-up. In the meantime, practising clinicians can have confidence and share with their patients that short-term lipid lowering therapy in older individuals, including with statins, is unlikely to have a major impact on cognition.”

Source: American College of Cardiology

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What Causes Us to Sneeze?

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A new study has identified, in mice, specific cells and proteins that control the sneeze reflex. 

Better understanding of what causes us to sneeze, and especially how neurons behave in response to allergens and viruses, may lead to treatments which can slow the spread of infectious respiratory diseases.

A tickle in the nose can help trigger a sneeze, which expels irritants and disease-causing pathogens. But the cellular pathways that control the sneeze reflex go far beyond the sinuses and have been poorly understood. Now, a team led by researchers at Washington University School of Medicine in St. Louis has identified, in mice, specific cells and proteins that control the sneeze reflex.

“Better understanding what causes us to sneeze — specifically how neurons behave in response to allergens and viruses — may point to treatments capable of slowing the spread of infectious respiratory diseases via sneezes,” said Qin Liu, PhD, an associate professor of anesthesiology and the study’s senior investigator.

“We study the neural mechanism behind sneezing because so many people, including members of my own family, sneeze because of problems such as seasonal allergies and viral infections,” explained Prof Liu, a researcher in the university’s Center for the Study of Itch and Sensory Disorders. “Our goal is to understand how neurons behave in response to allergies and viral infections, including how they contribute to itchy eyes, sneezing and other symptoms. Our recent studies have uncovered links between nerve cells and other systems that could help in the development of treatments for sneezing and for fighting infectious respiratory diseases.”

Sneezing is the most common and forceful way of spreading infectious droplets from respiratory infections. Over two decades ago, researchers discovered a sneeze-evoking region in the central nervous system, but since then there has been little progress in understanding the mechanism of the sneeze reflex at the cellular and molecular level.

For the new study, Prof Liu and her team used a mouse model to figure out which nerve cells send signals that make mice sneeze. The researchers exposed the mice to aerosolised droplets containing either histamine or capsaicin, a pungent compound made from chili peppers, both of which caused the mice to sneeze.

By examining nerve cells that already were known to react to capsaicin, Liu’s team was able to identify a class of small neurons linked to sneezing that was caused by that substance. The researchers then searched for neuropeptides that could transmit sneeze signals to those nerve cells, and hit upon a molecule called neuromedin B (NMB), which they found was required for sneezing.

By eliminating the NMD-sensitive neurons in the part of the nervous system that evoked sneezes in the mice, they blocked the sneeze reflex. Those neurons all make a protein called the neuromedin B receptor. In mice lacking that receptor, sneezing again was greatly reduced.

“Interestingly, none of these sneeze-evoking neurons were housed in any of the known regions of the brainstem linked to breathing and respiration,” Prof Liu said. “Although we found that sneeze-evoking cells are in a different region of the brain than the region that controls breathing, we also found that the cells in those two regions were directly connected via their axons, the wiring of nerve cells.”

By exposing part of the mouse brain to the NMB peptide, the researchers found they could directly stimulate the sneeze reflex, even though they had not been exposed to any capsaicin, histamine or other allergens.

Since many viruses and other pathogens are spread in part by aerosolised droplets, Prof Liu said it may be possible to limit the spread of those pathogens by targeting NMB or its receptor to limit sneezing in those known to be infected.

“A sneeze can create 20 000 virus-containing droplets that can stay in the air for up to 10 minutes,” Liu Prof explained. “By contrast, a cough produces closer to 3000 droplets, or about the same number produced by talking for a few minutes. To prevent future viral outbreaks and help treat pathological sneezing caused by allergens, it will be important to understand the pathways that cause sneezing in order to block them. By identifying neurons that mediate the sneeze reflex, as well as neuropeptides that activate these neurons, we have discovered targets that could lead to treatments for pathological sneezing or strategies for limiting the spread of infections.”

Source: Washington University School of Medicine

Journal information: Li, F., et al. (2021) Sneezing reflex is mediated by a peptidergic pathway from nose to brainstem. Cell. doi.org/10.1016/j.cell.2021.05.017.

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Call for More Neuroscience Research in Africa

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A team of neuroscientists are calling for greater support of neuroscience research in Africa based on an analysis of the continent’s past two decades of research outputs.  

The findings reveal important information about the nature of funding and international collaboration comparing activity in the continent to other countries, mainly the US, UK and areas of Europe. It is hoped that the study will provide useful data to help further develop science in Africa.  

The greatest human genetic diversity is found in Africa, and Eurasian genomes have less variation than African ones; in fact, Eurasian genomes can be considered a subset of African ones. This carries important implications for understanding human diseases, including neurological disorders.

Co-lead senior author Tom Baden, Professor of Neuroscience in the School of Life Sciences and the Sussex Neuroscience research group at the University of Sussex said: “One beautiful thing about science is that there is no such thing as a truly local problem. But that also means that there should be no such thing as a local solution – research and scientific communication by their very nature must be a global endeavour.  

“And yet, currently the vast majority of research across most disciplines is carried out by a relatively small number of countries, located mostly in the global north. This is a huge waste of human potential.”  

The team, made up of experts from the University of Sussex, the Francis Crick Institute and institutions from across Africa, analysed the entirety of Africa’s outputs in neuroscience over two decades. A lot of early neuroscience research took place in Egypt, it was pointed out.

Lead author Mahmoud Bukar Maina, a Research Fellow in the School of Life Sciences and the Sussex Neuroscience research group at the University of Sussex and visiting scientist at Yobe State University, Nigeria, explained: “Even though early progress in neuroscience began in Egypt, Africa’s research in this area has not kept pace with developments in the field around the world. There are a number of reasons behind this and, for the first time, our work has provided a clear picture of why – covering both strengths and weaknesses of neuroscience research in Africa and comparing this to other continents.  

“We hope it will provide useful data to guide governments, funders and other stakeholders in helping to shape science in Africa, and combat the ‘brain drain’ from the region.”  

Co-lead senior author Lucia Prieto-Godino, a Group Leader at the Francis Crick Institute, said: “One of the reasons why this work is so important, is that the first step to solve any problem is understanding it. Here we analyse key features and the evolution of neuroscience publications across all 54 African countries, and put them in a global context. This highlights strengths and weaknesses, and informs which aspects will be key in the future to support the growth and global integration of neuroscience research in the continent.” 

The study identifies the African countries with the greatest research outputs, revealing that most research funding originates from external sources such as the USA and UK.  

The researchers argue that a sustainable African neuroscience research environment needs local funding, suggesting that greater government backing is needed as well as support from the philanthropic sector.  
Professor Baden added: “One pervasive problem highlighted in our research was the marked absence of domestic funding. In most African countries, international funding far predominates. This is doubly problematic.  

“Firstly, it takes away the crucial funding stability that African researchers would need to meaningfully embark on large-scale and long-term research projects, and secondly, it means that the international, non-African funders essentially end up deciding what research is performed across the continent. Such a system would generate profound outrage across places like Europe – how then can it be acceptable for Africa?”

A number of the researchers involved in the study are members of TReND Africa, a charity supporting scientific capacity building in Africa.  

Source: University of Sussex

Journal information: M. B. Maina et al, Two decades of neuroscience publication trends in Africa, Nature Communications (2021). DOI: 10.1038/s41467-021-23784-8 , www.nature.com/articles/s41467-021-23784-8

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Free Will not Undermined by Neuroscience

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A new article argues that recent research undermines the notion that free will is an illusion, due to the buildup of brain activity before conscious movement.

Experiments from the 1960s to 1980s measured brain signals, leading many neuroscientists to believe that our brains make decisions before we do — that human actions were initiated by electrical waves, and therefore did not reflect free, conscious thought.

However, a new article in Trends in Cognitive Science argues that recent research undermines this contention against free will.

Study co-author Adina Roskies, and Helman Family Distinguished Professor, Dartmouth College, said: “This new perspective on the data turns on its head the way well-known findings have been interpreted. The new interpretation accounts for the data while undermining all the reasons to think it challenges free will.”

The debate over free will is mostly built on 1980s research using electroencephalograms to study brain activity. The EEG-based research measured when electrical signals begin to build in the brain, relative to when a person is aware of their desire to initiate a movement. The averaged data showed a buildup before movement that became known as the ‘readiness potential‘ (RP).

That research, conducted by neurophysiologist Benjamin Libet, contended that if the RP was present before a person had a conscious thought about moving, free will therefore could not be responsible for either the buildup of electrical signals or the subsequent movement.

This part of Libet’s logic was based on a likely false premise, the researchers argue.

“Because the averaged readiness potential reliably precedes voluntary movement, people assumed that it reflected a process specifically directed at producing that movement. As it turns out, and as our model has shown, that is not necessarily the case,” explained co-author Aaron Schurger, an assistant professor of psychology at Chapman University.

The article notes new research using computational modeling that indicates that the RP’s standard interpretation should be reassessed, especially in relation to the question of free will.

The study highlights findings suggesting that the RP — the pre-movement buildup of activity — reflects the neural activity that underlies the formation of a decision to move, as opposed to the outcome of a decision to move.

“These new computational models account for the consistent finding of the readiness potential without positing anything like an RP in individual trials. The readiness potential itself is a kind of artifact or illusion, one which would be expected to appear just as it does give the experimental design, but doesn’t reflect a real brain signal that begins with the RP onset or is read out by other areas,” said Prof Roskies.

Numerous challenges exist to the idea that the RP causes humans to act: isolating RP from other electrical signals in the brain; RP presence in tasks where motor activity is not needed; and ‘noise’ in analyses trying to confirm that RP initiates movement.

False positives, where RP is observed but fails to initiate movement, and inconsistencies in the lag between brain wave buildup and movement also complicate the understanding of the connection between the electrical activity in the brain and free will. Finally, there are philosophical implications to attempting to explore free will with brain data.

Source: Medical Xpress

Journal information: Aaron Schurger et al, What Is the Readiness Potential?, Trends in Cognitive Sciences (2021). DOI: 10.1016/j.tics.2021.04.001

Categories : General Interest NeurologyTags :

Researchers Discover that Humans can Readily Develop Echolocation Ability

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The ability for humans to sense their surrounding space with reflected sounds might sound like a superhero’s ability, but it is a skill that is developed by some blind people, who use clicks as a form of echolocation.

Echolocation is an ability known in dolphins, whales and bat species, which occurs when such animals emit a sound that reflects off objects in the environment, returning echoes that provide information about the surrounding space.

Existing research has shown that some blind people may use click-based echolocation to judge spaces and improve their navigation skills. Armed with this information, a team of researchers led by Dr Lore Thaler explored how people acquire this skill.

Over the course of a 10-week training programme, the team investigated how blindness and age affect learning of click-based echolocation. They also studied how learning this skill affects the daily lives of people who are blind.

Both blind and sighted people between 21 and 79 years of age participated in this study, which provided a training course of 10 weeks. Blind participants also took part in a 3-month follow up survey assessing how the training affected their daily life.

Both sighted and blind people improved considerably on all measures, and in some cases performed as well as expert echolocators did at the end of training. A surprising result was that a few sighted people even performed better than those who were blind.

However, neither age nor blindness limited participants’ rate of learning or in their ability to apply their echolocation skills to novel, untrained tasks.

Furthermore, in the follow up survey, all participants who were blind reported improved mobility, and 83% reported better independence and wellbeing.

Age or vision not a limitation

Overall, the results suggest that the ability to learn click-based echolocation is not strongly limited by age or level of vision. This has positive implications for the rehabilitation of people with vision loss or in the early stages of progressive vision loss.

Click-based echolocation is not presently taught as part of mobility training and rehabilitation for blind people. There is also the possibility that some people are reluctant to use click-based echolocation due to a perceived stigma around  the click sounds in social environments.

Despite this, the results indicate that both blind people who use echolocation and people new to echolocation are confident to use it in social situations, indicating that the perceived stigma is likely less than believed.

Source: Durham University

Journal information: Human click-based echolocation: Effects of blindness and age, and real-life implications in a 10-week training program, PLOS ONE (2021)

Categories : Injury & Trauma NeurologyTags :

White Matter Changes Uncovered in Repeated Brain Injury

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A new study has uncovered insights into white matter changes that occur during chronic traumatic encephalopathy (CTE), a progressive brain disease associated with repetitive head impacts. This discovery may help in identifying new targets for therapies.

CTE been diagnosed after death in the brains of American football players and other contact sport athletes as well as members of the armed services. The disease has been identified as causing impulsivity, explosivity, depression, memory impairment and executive dysfunction.

Though much prior research focused on repetitive head trauma leading to the development of abnormal tau, this study focused on white matter changes, particularly the oligodendrocytes which myelinate nerve sheaths. The results have been published online [PDF] in the journal Acta Neuropathologica.

“Research to date has focused on the deposition of abnormal tau in the gray matter in CTE. This study shows that the white matter undergoes important alterations as well.  There is loss of oligodendrocytes and alteration of oligodendrocyte subtypes in CTE that might provide new targets for prevention and therapies,” explained corresponding author Ann McKee, MD, chief of neuropathology at VA Boston Healthcare, director of the BU CTE Center.

Dr McKee and her team isolated cellular nuclei from the postmortem dorsolateral frontal white matter in eight cases of CTE and eight matched controls. They conducted single-nucleus RNA-seq (snRNA-seq) with these nuclei, revealing transcriptomic, cell-type-specific differences between the CTE and control cases. In doing so, they discovered that the white matter in CTE had fewer oligodendrocytes and the oligodendroglial subtypes were altered compared to control tissue.

Since previous studies have largely focused on the CTE-specific tau lesion located in the cortex in the brain, these findings are particularly informative as they explain a number of features of the disease. “In comparison, the cellular death process occurring in white matter oligodendrocytes in CTE appears to be separate from the accumulation of hyperphosphorylated tau,” she said. “We know that the behavioural and mood changes that occur in CTE are not explained by tau deposition. This study suggests that white matter alterations are also important features of the disease, and future studies will determine whether these white matter changes play a role in the production of behavioral or mood symptoms in CTE, such as explosivity, violence, impulsivity, and depression.”

Source: Boston University School of Medicine

Journal information: Chancellor, K. B., et al. (2021) Altered oligodendroglia and astroglia in chronic traumatic Encephalopathy. Acta Neuropathologica. doi.org/10.1007/s00401-021-02322-2.

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Autism Gene Impedes Neuron Development

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Researchers at the Institute of Science and Technology (IST) Austria have uncovered the role of a high-risk gene in autism spectrum disorder (ASD) and its important role during a critical phase of brain development.

Within the European Union alone, about three million people are affected by an autism spectrum disorder (ASD). Some are only mildly affected and can live independent lives. while others have severe disabilities. What the different forms have in common is difficulty with social interaction and communication, as well as repetitive-stereotypic behaviors. Mutations in a few hundred genes are associated with ASD. One of them is called Cullin 3, and it is a high-risk gene, and a mutation of it almost certainly leads to a disorder. 

To learn more about how the gene affects the brain, PhD students Jasmin Morandell and Lena Schwarz with Professor Gaia Novarino’s research group, turned to mice whose Cullin 3 gene has been partially switched off, comparing them to their healthy siblings. 

The three-chamber sociability test

In a series of behavioural and motoric tests, the team wanted to see if the modified mice mimicked some of the characteristics of patients with this form of autism and could therefore be used as model organisms. In one of these tests, the so-called three-chamber sociability test, a mouse could freely explore three adjacent chambers of a box connected by small doors. Two other mice were put in the outer boxes: One familiar to the studied mouse, the other mouse it had never met. “Healthy mice usually prefer the new over the already familiar mouse,” explained co-first author Jasmin Morandell. However, the mouse with the altered Cullin 3 gene, showed no recognition. The mice also had motor coordination deficits and other ASD-relevant cognitive impairments. This mouse model helped the researchers get to the heart of the problem. 

Dangerous protein buildup

While studying the mouse brain, the researchers noticed a very slight but consistent change in the position of some neurons. These neurons originate from a certain region in the brain, migrating toward the uppermost layers until they find their designated place in the cortex. The process is very sensitive, and even small changes in the speed at which they travel can alter the structure of the cortex. The scientists marked the migrating neurons to trace their movements. “We could observe migration deficits – the neurons are stranded in the lower cortex layers,” described the study’s other co-first author, Lena Schwarz. 

Malformations of the cortex
The reason for their poor movement lay in Cullin 3’s role in taggings old cells for degradation – a process that has to be tightly regulated to prevent proteins from accumulating. To find out which proteins are misregulated when Cullin 3 is defective, Morandell and Schwarz systematically analysed the protein composition of the mouse brain. “We were looking at proteins that accumulate in the mutant brain and found a protein called Plastin 3. Then Gaia [the professor they worked under] came across a poster describing the work of IST Austria’s Schur group in the hallway, and we got very excited,” said Jasmin Morandell. “They independently had been working on Plastin 3 as a regulator of cell motility and had complementary results to ours. That’s when we started working together,” Professor Gaia Novarino remembers.

The protein Plastin 3, which was previously unknown in the context of neuronal cell migration, turned out to have a key part in this process. “If the Cullin 3 gene is deactivated, the Plastin 3 protein accumulates, causing cells to migrate slower and over shorter distances. This is exactly what we saw happening in the cortex of the Cullin 3 mutant mice,” said Lena Schwarz.

Early developmental stage

All this occurs during a very early stage of brain development around halfway through pregnancy. “Determining these critical windows during brain development could be extremely important to fine-tune the treatment of patients with specific forms of ASD,” explained Prof Novarino, who is committed to improving diagnosis and treatment options for people with ASD. “Following up with the research on Plastin 3 could pave the way for some therapeutics. Inhibiting the accumulation of this protein could eventually alleviate some of the symptoms patients have,” Schwarz said.

 “We now know that defective Cullin 3 leads to increased levels of Plastin 3. This tight correlation shows that Plastin 3 protein levels may be an important factor for the control of cell-intrinsic movements,” said Jasmin Morandell. 

Source: IST Austria

Journal information: Jasmin Morandell, Lena A. Schwarz et al. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. DOI: 10.1038/s41467-021-23123-x

Categories : Mental Health NeurologyTags :

Lithium Brain Variations Play Role in Depression

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New research into depression has uncovered a previously unknown role played by the trace element lithium appears to play a role, which has been shown to be different in healthy and depressive people. 

Image source: Pixabay

Lithium is widely known from rechargeable batteries but is also known in psychiatry as a first-line mood stabiliser for bipolar disorders. lithium is present in drinking water in trace amounts. Studies have shown that a higher natural lithium content in drinking water is associated with a lower suicide rate among the population. However, the exact role lithium that plays in the brain is still not known.

Forensic medical experts at Ludwig-Maximilians-Universitaet (LMU) in Munich teamed up with physicists and neuropathologists at the Technical University of Munich (TUM) and an expert team from the Research Neutron Source Heinz Maier-Leibnitz (FRM II) to develop a technique which can be used to precisely map the distribution of lithium in the brain.

Neutrons probe for lithium

The scientists investigated the brain of a patient who was a suicidal and compared it with two control persons. The investigation focused on the ratio of the lithium concentration in white brain matter to the concentration in the gray matter of the brain.

In order to determine where how much lithium is present in the brain, the researchers analysed 150 samples from various brain regions—for example those regions which are presumably responsible for processing feelings. At the FRM II Prompt Gamma-Ray Activation Analysis (PGAA) instrument the researchers irradiated thin brain sections with neutrons.

“One lithium isotope is especially good at capturing neutrons; it then decays into a helium atom and a tritium atom,” explains Dr. Roman Gernhäuser of the Central Technology Laboratory of the TUM Department of Physics. The two decay products are picked up by detectors which provide lithium’s location in the brain sections. 

Since the lithium concentration in the brain is usually very low, it is also very difficult to ascertain. “Until now it wasn’t possible to detect such small traces of lithium in the brain in a spatially resolved manner,” said Dr Jutta Schöpfer of the LMU Munich Institute for Forensic Medicine. “One special aspect of the investigation using neutrons is that our samples are not destroyed. That means we can repeatedly examine them several times over a longer period of time,” Gernhäuser points out.

Significant differences

“We saw that there was significantly more lithium present in the white matter of the healthy person than in the gray matter. By contrast, the suicidal patient had a balanced distribution, without a measurable systematic difference,” Dr Roman Gernhäuser summarised.

“Our results are fairly groundbreaking, because we were able for the first time to ascertain the distribution of lithium under physiological conditions,” Schöpfer said

“Since we were able to ascertain trace quantities of the element in the brain without first administering medication and because the distribution is so clearly different, we assume that lithium indeed has an important function in the body.”

Only the beginning

“Of course the fact that we were only able to investigate brain sections from three persons marks only a beginning,” Gernhäuser said. “However, in each case we were able to investigate many different brain regions which confirmed the systematic behaviour.”

“We would be able to find out much more with more patients, whose life stories would also be better known,” said Gernhäuser, adding that then the question of whether lithium distribution was a cause or a result of depression.

Source: Medical Xpress

Categories : NeurologyTags :

Use of Robotic ‘Third Thumb’ Reorganises Brain Area

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Scientists have found that adding an extra robotic “thumb” worn by healthy individuals results in reorganisation and shrinkage of the brain region devoted to controlling the other thumb.

The findings come from ongoing research at University College London (UCL) into a 3D-printed robotic thumb known as “Third Thumb.” Worn on the dominant hand and operated by moving the big toe, volunteers equipped with them rapidly learned how to use the extra thumb to do all sorts of tasks—lifting, carrying, sorting and stacking multiple objects with their single enhanced hand.

However, MRI scans showed that after just a few days, participants’ brains had reorganised the natural hand’s ‘representation’ in a region associated with movement, effectively shrinking it. The researchers are not sure whether this is good or bad.

But they said it should give the growing field of ‘motor augmentation’ something to consider going forward.

Motor augmentation refers to robotic devices that can act as extra fingers or even a whole arm, with the aim of expanding the normal human movement capacity.

It might sound like science fiction but there a whole range of real applications, according to researcher Dani Clode, the designer of the Third Thumb.

She cited the example of factory workers or engineers who routinely perform repetitive but physically demand tasks.

“An extra pair of hands or digits could assist them in difficult assembly situations, allowing them to do their job in a more safe and efficient way, and perhaps without assistance from others,” Clode said.

Workers already make use of robotic exoskeletons to reduce strain in physically demanding tasks, such as working underneath cars in assembly lines.

Tamar Makin, a professor of cognitive neuroscience at UCL, said robotic appendages could be used in everything from high-precision scenarios—like surgery—to mundane chores.

“There are so many things we could do if we had hand extension,” Makin said. “We could chop vegetables while stirring a broth, or sip our coffee while typing. The opportunities are endless, but because this is such a novel concept—and because our world has been designed to accommodate our five-fingered two hands—people might struggle to imagine what it could be used for.”

Though these robotic upgrades offer so many possibilities, there are many unknowns. And these latest findings, published May 19 in the journal Science Robotics, raise questions.

Makin, Clode and their colleagues had 36 able-bodied volunteers learn to use the Third Thumb, performing tasks in and out the lab.

The device is worn on the pinkie side of the hand, attached by straps that wrap around the wrist and palm. The wearer operates it by manipulating sensors strapped under each big toe.

Despite that complicated-sounding toe-robot coordination, the study participants became adept at using the thumb over just five days, the researchers said.

Some change in the brain is expected because the additional thumb forced people to alter the way they moved their hand, Makin said.

“What surprised us is how quickly this happened,” she said. “After five days of practice to use the thumb, their own hand representation—which they’ve been developing over the course of their entire life—has changed.”

The ability to use their natural fingers showed no signs of degradation, but that is something they will monitor going forward.

Neurologist Dr Eran Klein, an affiliate assistant professor at the University of Washington, who studies the intersection of neurology and philosophy, said he was unsure how much weight to give the new study’s findings. “The brain changes all the time in response to learning skills,” Klein noted.

Still, he believes the study raises interesting questions. Broadly, Klein said, there’s the matter of “what is lost” when humans outsource skills to devices, such as losing navigational ability with the use of GPS. With robotic appendages, Klein said, one issue is whether they’re inherently different from any other tool people use—like a screwdriver.

He noted that since the devices are worn on the body and resemble human digits or limbs, so it probably does. The question is what happens to the ‘schema’ of the body, but there are examples — such as people who use a cane, for instance, can start to feel it’s part of them, Klein pointed out.

“I think what’s interesting about this study,” he said, “is that it brings up the bigger question of, what are we going to allow as things that become ‘part of us’?”

Source: Medical Xpress