Posts tagged science
Articles and news from the latest research reports.
Epileptic Seizures Can Propagate Using Functional Brain Networks
The seizures that affect people with temporal-lobe epilepsy usually start in a region of the brain called the hippocampus. But they are often able to involve other areas outside the temporal lobe, propagating via anatomically and functionally connected networks in the brain. New research findings that link decreased brain cell concentration to altered functional connectivity in temporal-lobe epilepsy are reported in an article in Brain Connectivity, a bimonthly peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available on the Brain Connectivity website.
Martha Holmes and colleagues from Vanderbilt University, Nashville, TN, identified regions in the brains of patients with temporal-lobe epilepsy that had reduced gray-matter concentrations. Greater reductions in gray-matter concentration correlated with either decreased or increased signaling and communication between brain regions connected through known functional networks.
The authors present their findings in the article “Functional Networks in Temporal-Lobe Epilepsy: A Voxel-Wise Study of Resting-State Functional Connectivity and Gray-Matter Concentration.”
“This is one of the first studies to actually correlate both functional and structural brain changes in epilepsy,” says Christopher Pawela, PhD, Co-Editor-in-Chief and Assistant Professor, Medical College of Wisconsin. “This is an exciting finding and may have impact in other brain disorders in which both the structure and function of the brain are involved.”
Feeling hungry may protect the brain against Alzheimer’s disease
The feeling of hunger itself may protect against Alzheimer’s disease, according to study published today in the journal PLOS ONE. Interestingly, the results of this study in mice suggest that mild hunger pangs, and related hormonal pathways, may be as important to the much-discussed value of “caloric restriction” as actually eating less.
Caloric restriction is a regimen where an individual consumes fewer calories than average, but not so few that they become malnourished. Studies in many species have suggested that it could protect against neurodegenerative disorders and extend lifespans, but the effect has not been confirmed in human randomized clinical trials.
Efforts to understand how cutting calories may protect the brain have grown increasingly important with news that American Alzheimer’s deaths are increasing, and because the best available treatments only delay onset in a subset of patients.
Study authors argue that hormonal signals are the middlemen between an empty gut and the perception of hunger in the brain, and that manipulating them may effectively counter age-related cognitive decline in the same way as caloric restriction.
“This is the first paper, as far as we are aware, to show that the sensation of hunger can reduce Alzheimer’s disease pathology in a mouse model of the disease,” said Inga Kadish, Ph.D., assistant professor in the Department of Cell, Developmental and Integrative Biology (CDIB) within the School of Medicine at the University of Alabama at Birmingham. “If the mechanisms are confirmed, hormonal hunger signaling may represent a new way to combat Alzheimer’s disease, either by itself or combined with caloric restriction.”
The team theorizes that feeling hungry creates mild stress. That, in turn, fires up metabolic signaling pathways that counter plaque deposits known to destroy nerve cells in Alzheimer’s patients. The idea is an example of hormesis theory, where damaging stressors like starvation are thought to be good for you when experienced to a lesser degree.
To study the sensation of hunger, the research team analyzed the effects of the hormone ghrelin, which is known to make us feel hungry. They used a synthetic form of ghrelin in pill form, which let them control dosage such that the ghrelin-treated mice felt steadily, mildly hungry.
If it could be developed, a treatment that affected biochemical pathways downstream of hunger signals might help delay cognitive decline without consigning people to a life of feeling hungry. Straight caloric restriction would not be tolerable for many persons over the long-run, but manipulating post-hunger signaling might.
This line of thinking becomes important because any protective benefit brought about by drugs or diets that mildly adjust post-hunger signals might be most useful if started in those at risk as early in life as possible. Attempts to treat the disease years later – when nerve networks are damaged enough for neurological symptoms to appear – may be too late. In the current study, it was long-term treatment with a ghrelin agonist that improved cognitive performance in mice tested when they had reached an advanced age.
Study details
The study looked at whether or not the feeling of hunger, in the absence of caloric restriction, could counter Alzheimer’s pathology in mice genetically engineered to have three genetic mutations known to cause the disease in humans.
Study mice were divided into three groups: one that received the ‘synthetic ghrelin’ (ghrelin agonist), a second that underwent caloric restriction (20 percent less food) and a third group that was fed normally. Study measures looked at each group’s ability to remember, their degree of Alzheimer’s pathology and their level of related, potentially harmful immune cell activation.
Results of such studies are most appropriately presented in terms of general trends in the data and statistical assessments of their likelihood if only chance factors were in play, a trait captured in each result’s P value (the smaller the better). Thus, the first formal result of the study are that, in mice with the human Alzheimer’s mutations, both the group treated with the ghrelin agonist LY444711 and the group that underwent caloric restriction performed significantly better in the a water maze than did than mice fed normally (p=0.023).
The water maze is the standard test used to measure mouse memory. Researchers put mice in a pool with an invisible platform on which they could rest, and measured how quickly the mice found the platform in a series of tests. Mice with normal memory will remember where the platform is, and find it more quickly each time they are placed in the pool. Ghrelin agonist-treated mice found the hidden platform 26 percent faster than control mice, with caloric restricted mice doing so 23 percent faster than control mice.
The second result was a measure of the buildup of a cholesterol-related protein called amyloid beta in the forebrain, an early step in the destruction of nerve cells that accompanies Alzheimer’s disease. The formal amyloid beta results show that mice either treated with the ghrelin agonist or calorically restricted had significantly less buildup of amyloid beta in the dentate gyrus, the part of the brain that controls memory function, than mice fed normally (i.e., control, 3.95±0.83; LY, 2.05±0.26 and CR, 1.28±0.17%, respectively; Wilcoxon p=0.04).
The above results translate roughly into a 67 percent reduction of this pathology in caloric-restricted mice as compared to control mice, and a 48 percent reduction of amyloid beta deposits when comparing the ghrelin-treated mice with the control group. These percentages are neither final nor translatable to humans, but are simply meant to convey the idea of “better.”
Finally, the team examined the difference in immune responses related to Alzheimer’s pathology in each of the three groups. Microglia are the immune cells of the brain, engulfing and removing invading pathogens and dead tissue. They have also been implicated in several diseases when their misplaced activation damages tissues. The team found that mice receiving the ghrelin agonist treatment had both reduced levels of microglial activation compared to the control group, similar to the effect of caloric restriction.
The ghrelin agonist used in the study does not lend itself to clinical use and will not play a role in the future prevention of Alzheimer’s disease, said Kadish. It was meant instead to prove a principle that hormonal hunger signaling itself can counter Alzheimer’s pathology in a mammal. The next step is to understand exactly how it achieved this as a prerequisite to future treatment design.
Ghrelin is known to create hunger signals by interacting with the arcuate nucleus in the part of the brain called the hypothalamus, which then sends out signaling neuropeptides that help the body sense and respond to energy needs. Studies already underway in Kadish’s lab seek to determine the potential role of these pathways and related genes in countering disease.
“Our group in the School of Public Health was studying whether or not a ghrelin agonist could make mice hungry as we sought to unravel mechanisms contributing to the life-prolonging effects of caloric restriction,” said David Allison, Ph.D., associate dean for Science in the UAB School of Public Health and the project’s initiator.
“Because of the interdisciplinary nature of UAB, our work with Dr. Allison led to an amazing conversation with Dr. Kadish about how we might combine our research with her longtime expertise in neurology because caloric restriction had been shown in early studies to counter Alzheimer’s disease,” said Emily Dhurandhar, Ph.D., a trainee in the UAB Nutrition Obesity Research Center and first study author. “The current study is the result.”
(Source: uab.edu)
Mental illness associated with heavy cannabis use
People with mental illnesses are more than seven times more likely to use cannabis weekly compared to people without a mental illness, according to researchers from the Centre for Addiction and Mental Health (CAMH) who studied U.S. data.
Cannabis is the most widely used illicit substance globally, with an estimated 203 million people reporting use. Although research has found links between cannabis use and mental illness, exact numbers and prevalence of problem cannabis use had not been investigated.
“We know that people with mental illness consume more cannabis, perhaps partially as a way to self- medicate psychiatric symptoms, but this data showed us the degree of the correlation between cannabis use, misuse, and mental illness,” said Dr. Shaul Lev-ran, Adjunct Scientist at CAMH and Head of Addiction Medicine at the Sheba Medical Center, Israel.
“Based on the number of individuals reporting weekly use, we see that people with mental illness use cannabis at high rates. This can be of concern because it could worsen the symptoms of their mental illness,” said Lev-ran, who conducted the research as a post-doctoral fellow with the Social Aetiology of Mental Illness (SAMI) Training Program at CAMH.
Researchers also found that individuals with mental illness were 10 times more likely to have a cannabis use disorder.
In this new study, published in the journal Comprehensive Psychiatry, CAMH researchers analyzed data from face-to-face interviews with over 43,000 respondents over the age of 18 from the National Epidemiologic Survey on Alcohol and Related Conditions. Using structured questionnaires, the researchers assessed cannabis use as well as various mental illnesses including depression, anxiety, drug and alcohol use disorders and personality disorders, based on criteria from the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).
Among those will mental illness reporting at least weekly cannabis use, rates of use were particularly elevated for those with bipolar disorder, personality disorders and other substance use disorders.
In total, 4.4 per cent of individuals with a mental illness in the past 12 months reported using cannabis weekly, compared to 0.6 per cent among individuals without any mental illness. Cannabis use disorders occurred among 4 per cent of those with mental illness versus 0.4 per cent among those without.
Researchers also noted that, although cannabis use is generally higher among younger people, the association between mental illness and cannabis use was pervasive across most age groups.
They emphasize the importance of screening for frequent and problem cannabis use among those with mental illness, so that targeted prevention and intervention may be employed.
Vitamin P as a potential approach for the treatment of damaged motor neurons
Biologists from the Ruhr-Universität Bochum have explored how to protect neurons that control movements from dying off. In the journal “Molecular and Cellular Neuroscience” they report that the molecule 7,8-Dihydroxyflavone, also known as vitamin P, ensures the survival of motor neurons in culture. It sends the survival signal on another path than the molecule Brain Derived Neurotrophic Factor (BDNF), which was previously considered a candidate for the treatment of motoneuron diseases or after spinal cord damage. “The Brain Derived Neurotrophic Factor only had a limited effect when tested on humans, and even had partially negative consequences”, says Prof. Dr. Stefan Wiese from the RUB Work Group for Molecular Cell Biology. “Therefore we are looking for alternative ways to find new approaches for the treatment of neurodegenerative diseases such as Amyotrophic Lateral Sclerosis.”
Same effect, different mode of action
In previous studies, researchers hypothesised that vitamin P is an analogue of BDNF and thus works in the same way. This theory has been disproved by the team led by Dr. Teresa Tsai and Prof. Stefan Wiese from the Group for Molecular Cell Biology and the Department of Cell Morphology and Molecular Neurobiology headed by Prof. Andreas Faissner. Both substances ensure that isolated motor neurons of the mouse survive in cell culture and grow new processes, but what exactly the molecules trigger at the protein level varies. BDNF activates two signalling pathways, the so-called MAP kinase and PI3K/AKT signal paths. Vitamin P on the other hand makes use only of the latter.
The dose is crucial
However, vitamin P only unfolded its positive effects on the motor neurons in a very small concentration range. “These results show how important an accurate determination of dose and effect is”, says Prof. Wiese. An overdose of vitamin P reduced the survival effect, and over a certain amount, no more positive effects occurred at all. The researchers hope that vitamin P could have less negative side effects than BDNF. “It is easier to use, because vitamin P, in contrast to BDNF, can pass the blood-brain barrier and therefore does not have to be introduced into the cerebrospinal fluid using pumps like BDNF,” says Wiese.
Speaking a tonal language (such as Cantonese) primes the brain for musical training
Non-musicians who speak tonal languages may have a better ear for learning musical notes, according to Canadian researchers.
Tonal languages, found mainly in Asia, Africa and South America, have an abundance of high and low pitch patterns as part of speech. In these languages, differences in pitch can alter the meaning of a word. Vietnamese, for example, has eleven different vowel sounds and six different tones. Cantonese also has an intricate six-tone system, while English has no tones.
Researchers at Baycrest Health Sciences’ Rotman Research Institute (RRI) in Toronto have found the strongest evidence yet that speaking a tonal language may improve how the brain hears music. While the findings may boost the egos of tonal language speakers who excel in musicianship, they are exciting neuroscientists for another reason: they represent the first strong evidence that music and language – which share overlapping brain structures – have bi-directional benefits!
The findings are published today in PLOS ONE, an international, peer-reviewed open-access science journal.
The benefits of music training for speech and language are already well documented (showing positive influences on speech perception and recognition, auditory working memory, aspects of verbal intelligence, and awareness of the sound structure of spoken words). The reverse – the benefits of language experience for learning music – has largely been unexplored until now.
"For those who speak tonal languages, we believe their brain’s auditory system is already enhanced to allow them to hear musical notes better and detect minute changes in pitch," said lead investigator Gavin Bidelman, who conducted the research as a post-doctoral fellow at Baycrest’s RRI, supported by a GRAMMY Foundation® grant.
"If you pick up an instrument, you may be able to acquire the skills faster to play that instrument because your brain has already built up these auditory perceptual advantages through speaking your native tonal language."
But Bidelman, now assistant professor with the Institute for Intelligent Systems and School of Communication Science & Disorders at the University of Memphis, was quick to dispel the notion that people who speak tonal languages make better musicians. Musicianship requires much more than the sense of hearing and plenty of English-speaking musical icons will put that quick assumption to rest.
That music and language – two key domains of human cognition – can influence each other offers exciting possibilities for devising new approaches to rehabilitation for people with speech and language deficits, said Bidelman.
"If music and language are so intimately coupled, we may be able to design rehabilitation treatments that use musical training to help individuals improve speech-related functions that have been impaired due to age, aphasia or stroke," he suggested. Bidelman added that similar benefits might also work in the opposite direction. Musical listening skills could be improved by designing well-crafted speech and language training programs.
The study
Fifty-four healthy adults in their mid-20s were recruited for the study from the University of Toronto and Greater Toronto Area. They were divided into three groups: English-speaking trained musicians (instrumentalists) and Cantonese-speaking and English-speaking non-musicians. Wearing headphones in a sound-proof lab, participants were tested on their ability to discriminate complex musical notes. They were assessed on measures of auditory pitch acuity and music perception as well as general cognitive ability such as working memory and fluid intelligence (abstract reasoning, thinking quickly).
While the musicians demonstrated superior performance on all auditory measures, the Cantonese non-musicians showed similar performance to musicians on music and cognitive behavioural tasks, testing 15 to 20 percent higher than that of the English-speaking non-musicians.
Bidelman added that not all tonal languages may offer the music listening benefits seen with the Cantonese speakers in his study. Mandarin, for example, has more “curved” tones and the pitch patterns vary with time – which is different from how pitch occurs in music. Musical pitch resembles “stair step, level pitch patterns” which happen to share similarities with the Cantonese language, he explained.
Study shows humans and apes learn language differently
How do children learn language? Many linguists believe that the stages that a child goes through when learning language mirror the stages of language development in primate evolution. In a paper published in the Proceedings of the National Academy of Sciences, Charles Yang of the University of Pennsylvania suggests that if this is true, then small children and non-human primates would use language the same way. He then uses statistical analysis to prove that this is not the case. The language of small children uses grammar, while language in non-human primates relies on imitation.
Yang examines two hypotheses about language development in children. One of these says that children learn how to put words together by imitating the word combinations of adults. The other states that children learn to combine words by following grammatical rules.
Linguists who support the idea that children are parroting refer to the fact that children appear to combine the same words in the same ways. For example, an English speaker can put either the determiner “a” or the determiner “the” in front of a singular noun. “A door” and “the door” are both grammatically correct, as are “a cat” and “the cat.” However, with most singular nouns, children tend to use either “a” or “the” but not both. This suggests that children are mimicking strings of words without understanding grammatical rules about how to combine the words.
Yang, however, points out that the lack of diversity in children’s word combinations could reflect the way that adults use language. Adults are more likely to use “a” with some words and “the” with others. “The bathroom” is more common than “a bathroom.” “A bath” is more common than “the bath.”
To test this conjecture, Yang analyzed language samples of young children who had just begun making two-word combinations. He calculated the number of different noun-determiner combinations someone would make if they were combining nouns and determiners independently, and found that the diversity of the children’s language matched this profile. He also found that the children’s word combinations were much more diverse than they would be if they were simply imitating word strings.
Yang also studied language diversity in Nim Chimpsky, a chimpanzee who knows American Sign Language. Nim’s word combinations are much less diverse than would be expected if he were combining words independently. This indicates that he is probably mimicking, rather than using grammar.
This difference in language use indicates that human children do not acquire language in the same way that non-human primates do. Young children learn rules of grammar very quickly, while a chimpanzee who has spent many years learning language continues to imitate rather than combine words based on grammatical rules.
BRAIN Initiative Launched to Unlock Mysteries of Human Mind
Today at the White House, President Barak Obama unveiled the “BRAIN” Initiative — a bold new research effort to revolutionize our understanding of the human mind and uncover new ways to treat, prevent, and cure brain disorders like Alzheimer’s, schizophrenia, autism, epilepsy, and traumatic brain injury.
The NIH Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is part of a new Presidential focus aimed at revolutionizing our understanding of the human brain. By accelerating the development and application of innovative technologies, researchers will be able to produce a revolutionary new dynamic picture of the brain that, for the first time, shows how individual cells and complex neural circuits interact in both time and space. Long desired by researchers seeking new ways to treat, cure, and even prevent brain disorders, this picture will fill major gaps in our current knowledge and provide unprecedented opportunities for exploring exactly how the brain enables the human body to record, process, utilize, store, and retrieve vast quantities of information, all at the speed of thought.
Why is the NIH BRAIN Initiative needed?
With nearly 100 billion neurons and 100 trillion connections, the human brain remains one of the greatest mysteries in science and one of the greatest challenges in medicine. Neurological and psychiatric disorders, such as Alzheimer’s disease, Parkinson’s disease, autism, epilepsy, schizophrenia, depression, and traumatic brain injury, exact a tremendous toll on individuals, families, and society. Despite the many advances in neuroscience in recent years, the underlying causes of most of neurological and psychiatric conditions remain largely unknown, due to the vast complexity of the human brain. If we are ever to develop effective ways of helping people suffering from these devastating conditions, researchers will first need a more complete arsenal of tools and information for understanding how the brain functions both in health and disease.
Why is now the right time for the NIH BRAIN Initiative?
In the last decade alone, scientists have made a number of landmark discoveries that now create the opportunity to unlock the mysteries of the brain. We have witnessed the sequencing of the human genome, the development of new tools for mapping neuronal connections, the increasing resolution of imaging technologies, and the explosion of nanoscience. These discoveries have yielded unprecedented opportunities for integration across scientific fields. For instance, by combining advanced genetic and optical techniques, scientists can now use pulses of light in animal models to determine how specific cell activities within the brain affect behavior. What’s more, through the integration of neuroscience and physics, researchers can now use high-resolution imaging technologies to observe how the brain is structurally and functionally connected in living humans.
While these technological innovations have contributed substantially to our expanding knowledge of the brain, significant breakthroughs in how we treat neurological and psychiatric disease will require a new generation of tools to enable researchers to record signals from brain cells in much greater numbers and at even faster speeds. This cannot currently be achieved, but great promise for developing such technologies lies at the intersections of nanoscience, imaging, engineering, informatics, and other rapidly emerging fields of science.
How will the NIH BRAIN Initiative work?
Given the ambitious scope of this pioneering endeavor, it is vital that planning for the NIH BRAIN Initiative be informed by a wide range of expertise and experience. Therefore, NIH is establishing a high level working group of the Advisory Committee to the NIH Director (ACD) to help shape this new initiative. This working group, co-chaired by Dr. Cornelia “Cori” Bargmann (The Rockefeller University) and Dr. William Newsome (Stanford University), is being asked to articulate the scientific goals of the BRAIN initiative and develop a multi-year scientific plan for achieving these goals, including timetables, milestones, and cost estimates.
As part of this planning process, input will be sought broadly from the scientific community, patient advocates, and the general public. The working group will be asked to produce an interim report by fall 2013 that will contain specific recommendations on high priority investments for Fiscal Year (FY) 2014. The final report will be delivered to the NIH Director in June 2014.
How will the NIH BRAIN Initiative be supported?
In total, NIH intends to allocate $40 million in FY14. Given the cross-cutting nature of this project, the NIH Blueprint for Neuroscience Research — an initiative spanning 14 NIH Institutes and Centers — will be the leading NIH contributor to its implementation in FY14. Of course, a goal this audacious will require ideas from the best scientists and engineers across many diverse disciplines and sectors. Therefore, NIH is working in close collaboration with other government agencies, including the Defense Advanced Research Projects Agency (DARPA) and the National Science Foundation (NSF). Strong interest has also been expressed by several private foundations, including the Howard Hughes Medical Institute, the Allen Institute for Brain Science, and The Kavli Foundation, and the Salk Institute for Biological Studies. Private industries have also expressed a high level of interest in participation in this groundbreaking initiative.
Obama proposes $100m to map the human brain
President Barack Obama on Tuesday asked Congress to spend $100 million next year on a new project to map the human brain in hopes of eventually finding cures for disorders like Alzheimer’s, epilepsy and traumatic injuries.
Obama said the so-called BRAIN Initiative could create jobs and eventually lead to answers to ailments including Parkinson’s and autism and help reverse the effect of a stroke. The president told scientists gathered in the White House’s East Room that the research has the potential to improve the lives of billions of people worldwide.
‘‘As humans we can identify galaxies light-years away,’’ Obama said. ‘‘We can study particles smaller than an atom, but we still haven’t unlocked the mystery of the three pounds of matter that sits between our ears.’’
BRAIN stands for Brain Research through Advancing Innovative Neurotechnologies. The idea, which Obama first proposed in his State of the Union address, would require the development of new technology that can record the electrical activity of individual cells and complex neural circuits in the brain ‘‘at the speed of thought,’’ the White House said.
Obama wants the initial $100 million investment to support research at the National Institutes of Health, the Defense Advanced Research Projects Agency and the National Science Foundation. He also wants private companies, universities and philanthropists to partner with the federal agencies in support of the research. And he wants a study of the ethical, legal and societal implications of the research.
The goals of the work are unclear at this point. A working group at NIH, co-chaired by Cornelia ‘‘Cori’’ Bargmann of The Rockefeller University and William Newsome of Stanford University, would work on defining the goals and develop a multi-year plan to achieve them that included cost estimates.
Forget about plaque when diagnosing Alzheimer’s Disease
An Australian study has shown that plaque, long considered to be the hallmark of Alzheimer’s disease, is one of the last events to occur in the Alzheimer’s brain. This finding will impact the current debate about how best to diagnose and treat Alzheimer’s disease.
PhD student Amanda Wright and Dr Bryce Vissel from Sydney’s Garvan Institute of Medical Research studied a mouse model of Alzheimer’s disease in order to identify early versus late disease mechanisms and markers.
The data, published online today in the journal PLOS ONE, suggest that plaques occur long after memory loss, so may not be a useful early pathological marker for Alzheimer’s disease.
The Investigators found that significant nerve cell loss and a range of brain pathologies, including inflammation, began at the same time as subtle memory problems appeared, early in the disease process. Plaques occurred much later, well after significant memory loss.
“Ever since Alois Alzheimer first described this disease in 1906, plaque has been regarded as the definitive Alzheimer’s diagnosis,” said project leader Dr Vissel.
“Just last year, the first ever method of plaque detection through positron emission tomography (PET) was introduced into the clinic to assist in the diagnosis of Alzheimer’s disease – precisely because plaque is regarded as the conclusive marker for Alzheimer’s disease. Our study suggests that this method may not be accurate in earlier disease stages.”
Dr Vissel said that many billions of dollars have been spent around the world in trying to develop markers and drugs to block the development of plaque. Several drug trials based on this idea have failed recently.
“Our study supports the increasingly common view that treatment should start much earlier in the disease process. It also suggests that brain inflammation and cell loss may be an earlier indicator of disease pathology than plaque and an alternative target for treatment.”
“In addition, what’s coming out in various studies is that mild cognitive impairment may be another early predictor of Alzheimer’s. This seems to fit perfectly with our findings, which show mild memory loss and behavioural changes at an early stage before plaque appears.”
“I can see that the development of some clever learning and language tests to test for early signs of cognitive impairment will be an important indicator of dementia, when combined with a range of yet to be developed tests.”
(Image: Getty Images)
The Centre for Face Processing Disorders at BU campaigns for greater recognition of face blindness
Imagine not being able to recognise your own child at nursery or even pick out your own face from a line-up of photos.
This is just how severe face blindness, or prosopagnosia, can be.
"In extreme cases, people might withdraw socially - become depressed, leave their job, or just suffer endless embarrassment," said Bournemouth University psychologist Dr Sarah Bate.
Dr Bate leads the Centre for Facial Processing Disorders at BU, which carries out research to advance understanding of the causes of prosopagnosia and develops training strategies that can help to improve face recognition skills.
The Centre is now campaigning for formal recognition of face blindness, and has launched an e-petition for the issue to be discussed in parliament.
"Children with prosopagnosia can find it really difficult to make friends because all children wear school uniforms in the UK - this takes away any external cues to recognition," said Dr Bate.
"If children with face blindness seem socially withdrawn, this is often misinterpreted as an indicator of other socio-emotional difficulties or behavioural problems because of the lack of professional awareness of prosopagnosia."
She added: “Because prosopagnosia is not a formally recognised disorder, many people are reluctant to inform their employer that they have the condition, despite it influencing their performance at work or their relations with colleagues and clients.
"Indeed, many people feel they would be discriminated against if managers became aware of their condition, and this may prevent promotion and impede other opportunities in the workplace."
You can sign the e-petition here
To find out more about face blindness and the work of the Centre for Face Processing Disorders visit: www.prosopagnosiaresearch.org
(Image: Allegro-Designs)