Posts tagged science

While reading, children and adults alike must avoid confusing mirror-image letters (like b/d or p/q). Why is it difficult to differentiate these letters? When learning to read, our brain must be able to inhibit the mirror-generalization process, a mechanism that facilitates the recognition of identical objects regardless of their orientation, but also prevents the brain from differentiating letters that are different but symmetrical. A study conducted by the researchers of the Laboratoire de Psychologie du Développement et de l’Education de l’Enfant (CNRS / Université Paris Descartes / Université de Caen Basse-Normandie) is available on the website of the Psychonomic Bulletin & Review (Online First Articles).

In recent years, many studies on the process of learning to read have been based on the neuronal recycling hypothesis: the reuse of old brain mechanisms in a new adaptive role —a kind of “biological trick.” Specifically, neurons that are originally dedicated to the rapid identification of objects in the environment, through the mirror-generalization process, are “repurposed” during childhood to specialize in the visual recognition of letters and words.

In this study, the researchers showed 80 young adults pairs of images, first two letters and then two animals, asking them to determine whether they were identical. The readers consistently spent more time determining that two animal images, when preceded by mirror-image letters, were indeed identical. This increase in response time is called “negative priming”: the readers had to inhibit the mirror-generalization process in order to distinguish letters like b/d or p/q. They then needed a little more time to reactivate this strategy when it became useful again to quickly identify animals.

These results show that even adults need to inhibit the mirror-generalization process to avoid reading errors. Children must therefore learn to inhibit this strategy when learning to read. A failure of cognitive inhibition during the recycling of visual neurons in the brain could thus be a factor in dyslexia— a direction worth exploring, in light of these findings.

(Source: www2.cnrs.fr)

New York University biologists have identified a mechanism that helps explain how the diversity of neurons that make up the visual system is generated.

“Our research uncovers a process that dictates both timing and cell survival in order to engender the heterogeneity of neurons used for vision,” explains NYU Biology Professor Claude Desplan, the study’s senior author.

The study’s other co-authors were: Claire Bertet, Xin Li, Ted Erclik, Matthieu Cavey, and Brent Wells—all postdoctoral fellows at NYU.

Their work, which appears in the latest issue of the journal Cell, centers on neurogenesis—the process by which neurons are created.

A central challenge in developmental neurobiology is to understand how progenitors—stem cells that differentiate to form one or more kinds of cells—produce the vast diversity of neurons, glia, and non-neuronal cells found in the adult Central Nervous System (CNS). Temporal patterning is one of the core mechanisms generating this diversity in both invertebrates and vertebrates. This process relies on the sequential expression of transcription factors into progenitors, each specifying the production of a distinct neural cell type.

In the Cell paper, the researchers studied the formation of the visual system of the fruit fly Drosophila. Their findings revealed that this process, which relies on temporal patterning of neural progenitors, is more complex than previously thought.

They demonstrate that in addition to specifying the production of distinct neural cell type over time, temporal factors also determine the survival or death of these cells as well as the mode of division of progenitors. Thus, temporal patterning of neural progenitors generates cell diversity in the adult visual system by specifying the identity, the survival, and the number of each unique neural cell type.

(Source: nyu.edu)

How nerve cells within the brain communicate with each other over long distances has puzzled scientists for decades. The way networks of neurons connect and how individual cells react to incoming pulses in principle makes communication over large distances impossible. Scientists from Germany and France provide now a possible answer how the brain can function nonetheless: by exploiting the powers of resonance.

(Image caption: Resonance in the activity of nerve cells (left) allows activity within the brain to travel over large distances, e.g. from the back of the head to the front during the processing of visual stimuli. Credit: Gunnar Grah/BrainLinks-BrainTools)

As Gerald Hahn, Alejandro F. Bujan and colleagues describe in the journal “PLoS Computational Biology”, the ability of networks of neurons to resonate can amplify oscillations in the activity of nerve cells, allowing signals to travel much farther than in the absence of resonance. The team from the cluster of excellence BrainLinks-BrainTools and the Bernstein Center at the University of Freiburg and the UNIC department of the French Centre national de la recherche scientifique in Gif-sur-Yvette created a computer model of networks of nerve cells and analyzed its properties for signal propagation.

Earlier propositions how information travels through the brain had the flaw of being biologically implausible. They either postulated strong connections between distant brain areas for which there was no evidence, or they required a global mechanism setting these distant parts of the brain into linked oscillations. However, nobody could explain how this could actually be implemented.

The simulation study of Hahn and Bujan required neither unrealistic network properties nor the existence of a pacemaker for the brain. Instead, they found that resonance could be the key to long-distance communication in networks with relatively few and weak connections, as it is the case in the brain. Not all nerve cells excite other cells; some inhibit the activity of others. This means that the activity in a network can oscillate around a certain level of activity as a result of the interplay of excitation and inhibition. These networks typically have preferred frequencies at which oscillations are particularly strong, just as a taut string on a violin has a preferred frequency. If the activity tunes into this frequency, pulses propagate much farther. As the scientists point out, the combination of oscillatory signals together with resonance induced amplification may be the only possible form of long distance communication in certain cases. They further suggest that a network’s ability to change its preferred frequency may play a role in the way how information is at times processed differently in the brain.

(Source: pr.uni-freiburg.de)

The failing in the work of nerve cells: An international team of researchers led by Prof. Dr. Chris Meisinger from the Institute of Biochemistry and Molecular Biology of the University of Freiburg has discovered how Alzheimer’s disease damages mitochondria, the powerhouses of the cell. For several years researchers have known that the cellular energy supply of brain cells is impaired in Alzheimer’s patients. They suspect this to be the cause of premature death of nerve cells that occurs in the course of the disease. Little is known about the precise cause of this neuronal cell death, and many approaches and attempts to find an effective therapy have failed to make an impact. What is certain is that a tiny protein fragment by the name of “amyloid-beta” plays a key role in the process. Meisinger, a member of the Cluster of Excellence BIOSS Centre for Biological Signalling Studies of the University of Freiburg, and his team have now demonstrated how this protein fragment blocks the maturation of protein machines that are responsible for the production of energy inside the cellular powerhouses. The researchers demonstrated this with the help of model organisms and with brain samples from Alzheimer’s patients. “The elucidation of this key component of the disease mechanism will enable us to develop new therapies and improve diagnostics in the future,” explains Meisinger. The findings were published in the journal Cell Metabolism.

Mitochondria are made up of around 1500 different proteins. Most of them need to migrate to the cellular powerhouses before taking up their work. This import is facilitated by a so-called signaling sequence – tiny protein extensions that transport the protein into the mitochondria. Once the protein is inside, the signaling sequence is normally removed. Dirk Mossmann and Dr. Nora Vögtle from Meisinger’s research team have now discovered that the amyloid-beta peptide prevents mitochondria from removing these signaling sequences. As a consequence, incomplete proteins accumulate in the mitochondria. Since the signaling sequences remain attached, the proteins are unstable and can no longer adequately carry out their function in energy metabolism. The researchers demonstrated that modified yeast cells producing the amyloid-beta protein generate less energy and accumulate more harmful substances.

In the brain, the mechanism probably leads to the death of nerve cells: The brain shrinks and the patient suffers from dementia. The researchers are currently developing an Alzheimer’s blood test to detect the accumulation of mitochondrial precursor proteins. They suspect that the mitochondrial alterations observed in nerve cells will also be detected in the blood cells of Alzheimer’s patients.

(Source: pr.uni-freiburg.de)

Brain networks break down similarly in rare, inherited forms of Alzheimer’s disease and much more common uninherited versions of the disorder, a new study has revealed.

Scientists at Washington University School of Medicine in St. Louis have shown that in both types of Alzheimer’s, a basic component of brain function starts to decline about five years before symptoms, such as memory loss, become obvious.

The breakdown occurs in resting state functional connectivity, which involves groups of brain regions with activity levels that rise and fall in coordination with each other. Scientists believe this synchronization helps the regions form networks that work together or stay out of each other’s way during mental tasks.

“The brain networks affected by inherited Alzheimer’s disease in a 30-year-old are very similar to the networks affected by uninherited Alzheimer’s disease in a 60-, 70- or 80-year-old,” said senior author Beau Ances, MD, PhD. “This affirms that what we learn by studying inherited Alzheimer’s, which appears at younger ages, will help us better understand and treat more common forms of the disease.”

The research appears online in JAMA Neurology.

According to Ances, the results show that functional connectivity may help scientists monitor the effects of treatment as patients progress through the transition between early disease and the first appearance of obvious symptoms.

“Right now, this period when functional connectivity begins breaking down is a time when family and loved ones may start noticing little changes in personality or mental function in someone with the disease, but not significant enough changes to cause real alarm,” Ances said. “The hope is that one day treatment already will be well underway before these sorts of changes begin — we want to slow or stop the damage caused by Alzheimer’s years earlier.”

Inherited Alzheimer’s disease can strike very early in life, causing symptoms in patients as young as their 30s or 40s. Identifying the mutations that cause these forms of the disease has helped scientists find proteins that become problematic in more common forms of Alzheimer’s, which typically appear decades later.

Researchers have long assumed that additional connections exist between inherited and uninherited Alzheimer’s disease, but until recently they have not had sufficient data to directly test many of those connections. Challenges have included the small number of people with inherited Alzheimer’s, and the slow development of both forms of the disease.

Scientists at the Charles F. and Joanne Knight Alzheimer’s Disease Research Center at Washington University began to tackle the first challenge five years ago by organizing the Dominantly Inherited Alzheimer’s Network (DIAN), an international network for identifying and studying families with inherited forms of the disease. The network now includes nearly 400 families.

To address the second challenge, Washington University researchers at the center have been gathering extensive health data on seniors through long-term projects such as the Healthy Aging and Senile Dementia Study, which is entering its 31st year.

These pools of data allowed Ances, an associate professor of neurology, to compare the effects of inherited and uninherited Alzheimer’s on functional connectivity. Scientists assess functional connectivity by scanning the brains of research participants while they daydream.

“The question was, where does the decline of functional connectivity fit in the whole picture of the development of Alzheimer’s disease?” Ances said. “And it clearly does have a place in the middle stages of the disease.”

That’s not the best place to look for an initial diagnosis, according to Ances. Ideally, scientists want to start treating Alzheimer’s disease as soon as possible. 

“What this does tell us, though, is that functional connectivity may help us track the progression of Alzheimer’s in patients who are first diagnosed when they’re beginning to show early signs of dementia,” he said.

(Source: news.wustl.edu)