Researchers at Karolinska Institute have charted a highly detailed molecular atlas of the foetal development of the brain.
The study, published in Nature, made use of single-cell technology which was performed on mice. In this way, researchers have identified almost 800 different cells that are active during foetal development – far more than previously known.
“Brain development is well described and the main cell types are known. What is new about our atlas is the high resolution and detail,” said Sten Linnarsson, head of research and professor at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet.
In their work, the researchers followed the brain development of the mice from day seven, when the brain is just forming, to the end of pregnancy on day 18.
Using single-cell technology, they were able to identify the detailed composition of the brain during foetal development: what cell types exist, how many cells of each type, and how this changes at the various stages of development.
The researchers also studied gene activity in each individual cell, classifying cells according to these activity patterns.
Creating a molecular atlas
The result is a molecular atlas that accurately illustrates how all cells in the brain develop from the early embryo. The atlas shows, for example, the way early neural stem cells first increase and then decrease in number, being replaced by transitional forms in several waves that eventually mature into ready-made neurons.
The researchers also demonstrated how early stem cell lines branch much like a family tree, giving rise to several different types of mature cells. The next step is mapping out atlases of the human brain, both in adults and during foetal development.
“Atlases like this are of great importance for research into the brain, both to understand brain function and its diseases. Cells are the body’s basic building blocks and the body’s diseases are always expressed in specific cells. Genes that cause serious diseases are found in all of the body’s cells, but they cause disease only in specific cells in the brain,” said Prof Linnarsson.
A new study adds to the growing body of evidence that decisions regarding moderate-to-severe traumatic brain injury (TBI) should not be made too soon after the injury, as a good prognosis can still emerge.
Researchers followed 484 patients with moderate-to-severe TBI and found that among the patients in a vegetative state, one quarter “regained orientation” — awareness of who, when and where they were — within 12 months of their injury.
“Withdrawal of life-sustaining treatment based on early prediction of poor outcome accounts for most deaths in patients hospitalised with severe TBI,” said senior author Geoffrey Manley, MD, PhD, noting that 64 of the 92 fatalities in the study occurred within two weeks of injury. Dr Manley is professor and vice chair of neurological surgery at UCSF and chief of neurosurgery at Zuckerberg San Francisco General Hospital.
“TBI is a life-changing event that can produce significant, lasting disability, and there are cases when it is very clear early on that a patient will not recover,” he said. “But results from this study show a significant proportion of our participants experienced major improvements in life functioning, with many regaining independence between two weeks and 12 months after injury.”
The patients in the study were enrolled by the brain injury research initiative TRACK-TBI, of which Dr Manley is the principal investigator. All patients were 17 and older and had presented to hospitals with level 1 trauma centers within 24 hours of injury. Their exams met criteria for either moderate TBI or severe TBI. The causes were falls, assault and primarily crashes involving a motor vehicle.
The patients, whose average ages were 35 in the severe TBI group (78 percent males) and 38 in the moderate TBI group (80 percent males), were assessed using the Glasgow Outcomes Scale Extended (GOSE), which ranges from 1 for death to 8 for “upper good recovery” and resumption of normal life. Impairment was also categorised with the Disability Rating Scale (DRS).
At two weeks post-injury, 93 percent of the severe TBI group and 79 percent of the moderate TBI group had moderate-to-severe disability, according to the DRS, and 80 percent had GOSE scores from 2 to 3, meaning they required assistance in basic everyday functioning.
But by 12 months, half of the severe TBI group and three-quarters of the moderate TBI group had GOSE scores of at least 4, indicating they could function independently at home for at least eight hours per day. Moreover, 19 percent of the severe TBI group had no disability, according to the DRS, and a further 14 percent had only mild injury, the researchers noted.
Most surprising were the findings for the 62 surviving patients who had been in a vegetative state. By the 12-month mark all patients had recovered consciousness and 1 in 4 had regained orientation. All but one survivor in this group recovered at least basic communication ability.
“These patients made the cut for favorable outcome,” said co-first author, Joseph Giacino, PhD, of Spaulding Rehabilitation Hospital, Massachusetts General Hospital and Harvard Medical School. “Their GOSE scores were 4 or higher, which meant they could be at home unsupervised for at least eight hours a day, since they were able to take care of basic needs, such as eating and toileting.”
In prior work, a significant percentage of patients with grave impairments had been shown to achieve favorable functionality after many months or years. This study coincided with the recommendation in 2018 from the American Academy of Neurology that in the first 28 days after injury, clinicians should refrain from telling families that a patient’s prognosis is beyond hope.
“While a substantial proportion of patients die or suffer lasting disability, our study adds to growing evidence that severe acute impairment does not portend uniformly poor long-term outcome,” said Manley, who is also affiliated with the UCSF Weill Institute for Neurosciences. “Even those patients in a vegetative state – an outcome viewed as dire – may improve, since this is a dynamic condition that evolves over the first year.”
A Chinese study has found that the ability to sense nervous signals such as heartbeat varies with age, peaking in young adulthood, but does not seem to be associated with autism.
Interoception is the ability to process and integrate internal signals originating from one’s body, such as heartbeats and breathing patterns. This ability is important for maintaining homeostasis. Recent findings have suggested that autism spectrum disorders are associated with a wide range of sensory integration impairments including interoceptive accuracy.
However, it is still not clear whether individuals with subclinical features of autism, which only moderately impact daily life, also exhibit similar impairments in interoceptive accuracy. It is also not clear how interoceptive ability and its association with autistic traits varies with age.
In order to address this issue, Dr Raymond Chan’s team from the Institute of Psychology of the Chinese Academy of Sciences (CAS) has developed an innovative paradigm involving eye-tracking measures to examine the multidimensional interoception and autistic traits in different age groups.
In so doing, they recruited 114 healthy university students aged 19–22 and explored the correlations among autistic traits and interoceptive accuracy using an “Eye-tracking Interoceptive Accuracy Task” (EIAT), which presents two bouncing shapes and requires participants to look at the one whiches bounces in time with their heartbeat.
Since this task requires no verbal report or button-pressing, it enables the exploration of interoceptive accuracy in preschool children and individuals with psychiatric disorders or speech impairments.
However, while autistic traits correlated significantly with the ability to describe and express emotion (alexithymia) but not with the different dimensions of interoception such as interoceptive accuracy (performance of interoceptive ability on behavioural tests), interoceptive sensibility (subjective sensitivity to internal sensations on self-report questionnaires) and interoceptive awareness (personal insight into interoceptive aptitude).
They then recruited 52 preschool children aged four to six, 50 adolescents aged 12–16 and 50 adults aged 23–54 to specifically examine the relationship of autistic traits and interoceptive accuracy across these three age groups. The researchers found that interoceptive accuracy evolves from childhood to early adulthood, and then declines with age. The highest average accuracy was seen in 12-16 year olds. The dataset showed that the developmental trajectory of interoceptive accuracy has a reverted U-shape trend peaking around early adulthood.
The findings suggest that interoceptive accuracy significantly differs between typically-developing preschool children, adolescents and adults. The study also highlights the need for future study into preschool children with suspected autism spectrum disorders.
Dopamine can help explain both autistic behaviours and men’s need for motivation or ‘passion’ in order to succeed compared to women’s ‘grit’, according to a new study.
Men – more often than women – need passion to succeed at things. At the same time, boys are diagnosed as being on the autism spectrum four times as often as girls. Both statistics may be related to dopamine, one of our body’s neurotransmitters.
“This is interesting. Research shows a more active dopamine system in most men” than in women, says Hermundur Sigmundsson, a professor at the Norwegian University of Science and Technology’s (NTNU) Department of Psychology.
He is behind a new study addressing gender differences in key motivating factors to excel in something. The study uses men’s and women’s differing activity in the dopamine system as an explanatory model. The study enrolled 917 participants aged 14 to 77, consisting of 502 women and 415 men.
“We looked at gender differences around passion, self-discipline and positive attitude,” said Prof Sigmundsson. The study refers to these qualities as passion, grit and mindset. The researchers also applied theories to possible links with dopamine levels. Dopamine, a neurotransmitter that is released in the brain, is linked to learning, attention and our ability to focus. It can contribute to a feeling of satisfaction.
Men generally secrete more dopamine, but it plays a far more complex role than simply being a ‘happy hormone’. Dopamine is linked to learning, attention and our ability to focus.Previous studies on Icelandic students have shown that men are more dependent on passion in order to succeed at something. This study confirms the earlier findings. In six out of eight test questions, men score higher on passion than women.
However, the association with dopamine levels has not been established previously.
“The fact that we’ve developed a test to measure passion for goal achievement means that we can now relate dopamine levels to passion and goal achievement,” explained Prof Sigmundsson.
Women, on the other hand, may have greater self-discipline – or grit – and be more conscientious, according to other studies. Their level of passion may not be as pronounced in general, but they are also able to use this to excel.
The results for the women, however, are somewhat more ambiguous than men’s need to have a passion for something, and this study found no such gender difference. Nor did the researchers find any difference between the sexes in terms of growth mindset.
Previous studies have associated the dopamine system with many different conditions, such as ADHD, psychoses, manias and Parkinson’s disease. However, it may also be related to a certain form of autistic behaviour.
Some individuals with autism may develop a deep interest in certain topics, something which others may find strange or even off putting. People on the autism spectrum can focus intensely on these topics or pursuits, at least for a while, and dopamine may play a role in this.
“Other research in neuroscience has shown hyperactivity in the dopamine system in individuals with autism, and boys make up four out of five children on the autism spectrum. This, and dopamine’s relationship to passion, might be a mechanism that helps to explain this behaviour,” concluded Prof Sigmundsson.
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.
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.”
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.”
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.
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
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.
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.