Infant Cooing, Babbling Linked to Hearing Ability

Infants’ vocalizations throughout the first year follow a set of predictable steps from crying and cooing to forming syllables and first words. However, previous research had not addressed how the amount of vocalizations may differ between hearing and deaf infants. Now, University of Missouri research shows that infant vocalizations are primarily motivated by infants’ ability to hear their own babbling. Additionally, infants with profound hearing loss who received cochlear implants to help correct their hearing soon reached the vocalization levels of their hearing peers, putting them on track for language development.

“Hearing is a critical aspect of infants’ motivation to make early sounds,” said Mary Fagan, an assistant professor in the Department of Communication Science and Disorders in the MU School of Health Professions. “This study shows babies are interested in speech-like sounds and that they increase their babbling when they can hear.”

Fagan studied the vocalizations of 27 hearing infants and 16 infants with profound hearing loss who were candidates for cochlear implants, which are small electronic devices embedded into the bone behind the ear that replace some functions of the damaged inner ear. She found that infants with profound hearing loss vocalized significantly less than hearing infants. However, when the infants with profound hearing loss received cochlear implants, the infants’ vocalizations increased to the same levels as their hearing peers within four months of receiving the implants.

“After the infants received their cochlear implants, the significant difference in overall vocalization quantity was no longer evident,” Fagan said. “These findings support the importance of early hearing screenings and early cochlear implantation.”

Fagan found that non-speech-like sounds such as crying, laughing and raspberry sounds, were not affected by infants’ hearing ability. She says this finding highlights babies are more interested in speech-like sounds since they increase their production of those sounds such as babbling when they can hear.

“Babies learn so much through sound in the first year of their lives,” Fagan said. “We know learning from others is important to infants’ development, but hearing allows infants to explore their own vocalizations and learn through their own capacity to produce sounds.”

In future research, Fagan hopes to study whether infants explore the sounds of objects such as musical toys to the same degree they explore vocalization.

Fagan’s research, “Frequency of vocalization before and after cochlear implantation: Dynamic effect of auditory feedback on infant behavior,” was published in the Journal of Experimental Child Psychology.

Identification of a protein that may increase the currently short therapeutic window in stroke

A new study published in the prestigious publication The EMBO Journal shows that the mitochondrial protein Mfn2 may be a future therapeutic target for neuronal death reduction in the late phases of an ischemic stroke. The study has been coordinated by Dr Francesc Soriano, Ramón y Cajal researcher at the Department of Cell Biology of the University of Barcelona (UB) and member of the Research Group Celltec UB. The study, funded by the Fundació La Marató de TV3, is part of the PhD thesis developed by Àlex Martorell Riera (UB), first author of the article. Experts Antonio Zorzano and Manuel Palacín, from the Department of Biochemistry and Molecular Biology of UB and the Institute for Research in Biomedicine (IRB Barcelona), and Jesús Pérez Clausell and Manuel Reina, from the Department of Cell Biology of UB, also collaborated in the study.

When blood flow is blocked in the brain

According to the World Health Organization (WHO), strokes are the second leading cause of death in the world. A stroke occurs when a blood vessel is blocked interrupting blood flow in the brain. Ictus damage is progressive: it begins some minutes after the attack. Recommended treatment consists in restoring blood flow to the brain, but it must be done during the first four hours after the stroke.

According to researcher Francesc Soriano, “one of the main causes of brain death in ictus events is glutamate increase; glutamate is the main excitatory neurotransmitter in the central nervous system. Glutamate extracellular concentrations remain low due to the activity of membrane transporters, which require energy to work”.

When blood flow is blocked, energy levels are reduced in the affected area. This phenomenon leads glutamate transporters to work inversely, so glutamate is expelled to the extracellular space. Glutamate activates its receptors —particularly, the N-methyl-D-aspartate receptor (NMDA)— on neurons’ surface, a process that triggers an excessive flux of calcium, the activation of a series of reactions and neuronal death, in a process known as excitotoxicity. “Many of these excitotoxic cascades —points out Soriano— converge on the mitochondrion, an organelle which plays a major role not only in energy production, but also in apoptosis”.

New therapeutic strategies against ischemic ictus

Specifically, Mfn2 is a mitochondrial protein involved in the regulation of organelles’ morphology and function. The team led by Dr Francesc Soriano has just discovered that the reduction in Mfn2 protein levels occurs four hours after the initiation of the excitotoxic process in in vitro and in vivo animal models.

In vivo experiments proved that if Mfn2 reduction is stopped, delayed excitotoxic cell death is blocked. The research team from the Department of Cell Biology of UB found that the Mfn2 reduction is triggered by a genetic transcription mechanism (DNA is transcribed into RNA molecules). UB experts also discovered that MEF2 is the transcription factor involved in this process. Authors affirm that these findings are essential to find a strategy to reverse Mfn2 reduction.

Currently, the team led by Dr Francesc Soriano are researching on brain damage in excitotoxic conditions in animal models where the gene Mfn2 has been removed. The main objective is to design therapeutic strategic in order to reduce damage.

Presence or absence of early language delay alters anatomy of the brain in autism

A new study led by researchers from the University of Cambridge has found that a common characteristic of autism – language delay in early childhood – leaves a ‘signature’ in the brain. The results are published today (23 September) in the journal Cerebral Cortex.

The researchers studied 80 adult men with autism: 38 who had delayed language onset and 42 who did not. They found that language delay was associated with differences in brain volume in a number of key regions, including the temporal lobe, insula, ventral basal ganglia, which were all smaller in those with language delay; and in brainstem structures, which were larger in those with delayed language onset.

Additionally, they found that current language function is associated with a specific pattern of grey and white matter volume changes in some key brain regions, particularly temporal, frontal and cerebellar structures.

The Cambridge researchers, in collaboration with King’s College London and the University of Oxford, studied participants who were part of the MRC Autism Imaging Multicentre Study (AIMS).

Delayed language onset – defined as when a child’s first meaningful words occur after 24 months of age, or their first phrase occurs after 33 months of age – is seen in a subgroup of children with autism, and is one of the clearest features triggering an assessment for developmental delay in children, including an assessment of autism.

“Although people with autism share many features, they also have a number of key differences,” said Dr Meng-Chuan Lai of the Cambridge Autism Research Centre, and the paper’s lead author. “Language development and ability is one major source of variation within autism. This new study will help us understand the substantial variety within the umbrella category of ‘autism spectrum’. We need to move beyond investigating average differences in individuals with and without autism, and move towards identifying key dimensions of individual differences within the spectrum.”

He added: “This study shows how the brain in men with autism varies based on their early language development and their current language functioning. This suggests there are potentially long-lasting effects of delayed language onset on the brain in autism.”

Last year, the American Psychiatric Association removed Asperger Syndrome (Asperger’s Disorder) as a separate diagnosis from its diagnostic manual (DSM-5), and instead subsumed it within ‘autism spectrum disorder.’ The change was one of many controversial decisions in DSM-5, the main manual for diagnosing psychiatric conditions.

“This new study shows that a key feature of Asperger Syndrome, the absence of language delay, leaves a long lasting neurobiological signature in the brain,” said Professor Simon Baron-Cohen, senior author of the study. “Although we support the view that autism lies on a spectrum, subgroups based on developmental characteristics, such as Asperger Syndrome, warrant further study.”

“It is important to note that we found both differences and shared features in individuals with autism who had or had not experienced language delay,” said Dr Lai. “When asking: ‘Is autism a single spectrum or are there discrete subgroups?’ - the answer may be both.”

Dying brain cells cue new brain cells to grow in songbird

Brain cells that multiply to help birds sing their best during breeding season are known to die back naturally later in the year. For the first time researchers have described the series of events that cues new neuron growth each spring, and it all appears to start with a signal from the expiring cells the previous fall that primes the brain to start producing stem cells.

If scientists can further tap into the process and understand how those signals work, it might lead to ways to exploit these signals and encourage replacement of cells in human brains that have lost neurons naturally because of aging, severe depression or Alzheimer’s disease, said Tracy Larson, a University of Washington doctoral student in biology. She’s lead author of a paper in the Sept. 23 Journal of Neuroscience on brain cell birth that follows natural brain cell death.

Neuroscientists have long known that new neurons are generated in the adult brains of many animals, but the birth of new neurons – or neurogenesis – appears to be limited in mammals and humans, especially where new neurons are generated after there’s been a blow to the head, stroke or some other physical loss of brain cells, Larson said. That process, referred to as “regenerative” neurogenesis, has been studied in mammals since the 1990s.

This is the first published study to examine the brain’s ability to replace cells that have been lost naturally, Larson said.

“Many neurodegenerative disorders are not injury-induced,” the co-authors write, “so it is critical to determine if and how reactive neurogenesis occurs under non-injury-induced neurodegenerative conditions.”

The researchers worked with Gambel’s white-crowned sparrows, a medium-sized species 7 inches (18 centimeters) long that breeds in Alaska, then winters in California and Mexico. Sometimes in flocks of more than 100 birds, they can be so plentiful in parts of California that they are considered pests. The ones in this work came from Eastern Washington.

Like most songbirds, Gambel’s white-crowned sparrows experience growth in the area of the brain that controls song output during the breeding season when a superior song helps them attract mates and define their territories. At the end of the season, probably because having extra cells exacts a toll in terms of energy and steroids they require, the cells begin dying naturally and the bird’s song degrades.

Gambel’s white-crowned sparrows are particularly good to work with because their breeding cycle is closely tied to the amount of sunlight they receive. Give them 20 hours of light in the lab, along with the right increase of steroids, and they are ready to breed. Cut the light to eight to 12 hours and taper the steroids, the breeding behavior ends.

“As the hormone levels decrease, the cells in the part of the brain controlling song no longer have the signal to ‘stay alive,’” Larson said. “Those cells undergo programmed cell death – or cell suicide as some call it. As those cells die it is likely they are releasing some kind of signal that somehow gets transmitted to the stem cells that reside in the brain. Whatever that signal is then triggers those cells to divide and replace the loss of the cell that sent the signal to begin with.”

The next spring, all that’s needed is for steroids to ramp up and new cells start to proliferate in the song center of the brain.

“This paper doesn’t describe the exact nature of the signals that stimulate proliferation,” Larson said. “We’re just describing the phenomenon that there is this connection between cells dying and this stem cell proliferation. Finding the signal is the next step.”

“Tracy really nailed this down by going in and blocking cell death at the end of the breeding season,” said Eliot Brenowitz, UW professor of psychology and of biology, and co-author on the paper. “There are chemicals you can use to turn off the cell suicide pathway. When this was done, far fewer stem cells divided. You don’t get that big uptick in new neurons being born. That’s important because it shows there’s something about the cells dying that turns on the replacement process.’

“There’s no reason to think what goes on in a bird brain doesn’t also go on in mammal brains, in human brains,” Brenowitz said. “As far as we know, the molecules are the same, the pathways are the same, the hormones are the same. That’s the ultimate purpose of all this, to identify these molecular mechanisms that will be of use in repairing human brains.”

In mammals, the area of the brain that controls the sense of smell and the one that is thought to have a role in memories can produce tiny numbers of new brain cells but it is not understood how or why. The numbers of new cells is so low that trying to identify and quantify whether dying cells are being replaced and if so, the steps that are involved, is much more difficult than when using a songbird like Gambel’s white-crowned sparrow, Larson and Brenowitz said.

Blood test may help determine who is at risk for psychosis

A study led by University of North Carolina at Chapel Hill researchers represents an important step forward in the accurate diagnosis of people who are experiencing the earliest stages of psychosis.

Psychosis includes hallucinations or delusions that define the development of severe mental disorders such as schizophrenia. Schizophrenia emerges in late adolescence and early adulthood and affects about 1 in every 100 people. In severe cases, the impact on a young person can be a life compromised, and the burden on family members can be almost as severe.

The study published in the journal Schizophrenia Bulletin reports preliminary results showing that a blood test, when used in psychiatric patients experiencing symptoms that are considered to be indicators of a high risk for psychosis, identifies those who later went on to develop psychosis.

“The blood test included a selection of 15 measures of immune and hormonal system imbalances as well as evidence of oxidative stress,” said Diana O. Perkins, MD, MPH, professor of psychiatry in the UNC School of Medicine and corresponding author of the study. She is also medical director of UNC’s Outreach and Support Intervention Services (OASIS) program for schizophrenia.

“While further research is required before this blood test could be clinically available, these results provide evidence regarding the fundamental nature of schizophrenia, and point towards novel pathways that could be targets for preventative interventions,” Perkins said.

Clark D. Jeffries, PhD, bioinformatics scientist at the UNC-based Renaissance Computing Institute (RENCI), is a co-author of the study, which was conducted as part of the North American Prodrome Longitudinal Study (NAPLS), an international effort to understand risk factors and mechanisms for development of psychotic disorders. 

“Modern, computer-based methods can readily discover seemingly clear patterns from nonsensical data,” said Jeffries. “Added to that, scientific results from studies of complex disorders like schizophrenia can be confounded by many hidden dependencies. Thus, stringent testing is necessary to build a useful classifier. We did that.”

The study concludes that the multiplex blood assay, if independently replicated and if integrated with studies of other classes of biomarkers, has the potential to be of high value in the clinical setting.

(Image: Shutterstock)

Neuroscientists challenge long-held understanding of the sense of touch

Different types of nerves and skin receptors work in concert to produce sensations of touch, University of Chicago neuroscientists argue in a review article published Sept. 22, 2014, in the journal Trends in Neurosciences. Their assertion challenges a long-held principle in the field — that separate groups of nerves and receptors are responsible for distinct components of touch, like texture or shape. They hope to change the way somatosensory neuroscience is taught and how the science of touch is studied.

Sliman Bensmaia, PhD, assistant professor of organismal biology and anatomy at the University of Chicago, and Hannes Saal, PhD, a postdoctoral scholar in Bensmaia’s lab, reviewed more than 100 research studies on the physiological basis of touch published over the past 57 years. They argue that evidence once thought to show that different groups of receptors and nerves, or afferents, were responsible for conveying information about separate components of touch to the brain actually demonstrates that these afferents work together to produce the complex sensation.

"Any time you touch an object, all of these afferents are active together," Bensmaia said. "They each convey information about all aspects of an object, whether it’s the shape, the texture, or its motion across the skin."

Three different types of afferents convey information about touch to the brain: slowly adapting type 1 (SA1), rapidly adapting (RA) and Pacinian (PC). According to the traditional view, SA1 afferents are responsible for communicating information about shape and texture of objects, RA afferents help sense motion and grip control, and PC afferents detect vibrations.

In the past, Bensmaia said, this classification system has been supported by experiments using mechanical devices to elicit one or more of these specific components of touch. For example, responses to texture are often generated using a rotating, cylindrical drum covered with a Braille-like pattern of raised dots. Study subjects would place a finger on the drum as it rotated, and scientists recorded the neural responses.

Such experiments showed that SA1 afferents responded very strongly to this artificial stimulus, and RA and PC afferents did not, thus the association of SA1s with texture. However, in experiments in which subjects moved a finger across sandpaper — the quintessential example of the type of textures we encounter in the real world — SA1 afferents did not respond at all.

Bensmaia also pointed out discrepancies in the predominant thinking about how we discern shape. Perception of shapes has generally been tested using devices with raised or embossed letters to test a subject’s ability to interpret text by touch. These experiments also showed that such inputs produced a strong SA1 response, so they were implicated in perception of shape as well.

In the 1980s, however, researchers developed a device meant to help blind people read by generating vibrating patterns in the shape of letters on an array of pins. While the device was not a commercial success, people were able to use it to detect letter shapes and read, although experiments showed that it activated RA and PC afferents, not the supposedly shape-detecting SA1s.

Bensmaia said such experiments show how devices created to generate artificial stimuli focusing on individual components of the sense of touch can result in misleading findings. Some types of afferents are better than others at detecting texture or shape, for example, but all of them respond in their own way and contribute to the overall sensation.

"To get a good picture of how stimulus information is being conveyed in these afferent populations, you have to look at a diverse set of stimuli that spans the range of what you might feel in everyday tactile experience," he said.

Instead of thinking of individual groups of afferents working separately to process different components of the sense of touch, Bensmaia said we should think of all of them working in concert, much like individual musicians in a band to create its overall sound. Each musician contributes in his or her own way. Emphasizing one instrument or removing another can change the character of a song, but no single sound is responsible for the entire performance.

Adopting this new way of thinking will have far-reaching implications for both the study of the sense of touch and the design of future research, Bensmaia said.

"I think it’s going to change neuroscience textbooks, and by extension it’s going to change the way somatosensory neuroscience is taught. It’s really the starting point for everything."