Tag Archives: Activation

Very young children use both sides of the brain to process language, while adults only use half

New research could uncover why children recover more easily from neural injury compared to adults.

Examples of individual activation maps in each of the age groups in the study.
Image credits Elissa Newport.

Very young human brains use both their hemispheres to process language , a new paper reports. The study focused on computer imaging to see which parts of infants’ and young children’s brains handle such tasks. According to the findings, the whole brain pitches in, rather than a single hemisphere as is the case for adults.

Whole-brain experience

“Use of both hemispheres provides a mechanism to compensate after a neural injury,” says lead author Elissa Newport, Ph.D, a neurology professor at Georgetown University. “For example, if the left hemisphere is damaged from a perinatal stroke—one that occurs right after birth—a child will learn language using the right hemisphere. A child born with cerebral palsy that damages only one hemisphere can develop needed cognitive abilities in the other hemisphere. Our study demonstrates how that is possible.”

Human adults almost universally process language in their left hemisphere, a process known as ‘lateralization’. This has been shown by previous studies using brain imaging as well as from observing patients who suffered a stroke in their left hemispheres (and lost the ability to do so).

Very young children, however, don’t seem to do the same. Damage to either hemisphere of their brains is unlikely to result in language deficits, and they have been noted to recover language even after heavy damage to their left hemispheres. Why this happened, however, was unclear.

“It was unclear whether strong left dominance for language is present at birth or appears gradually during development,” explains Newport.

The team used functional magnetic resonance imaging (fMRI) to show that adult lateralization patterns aren’t established during our early days. Specific brain networks which cause lateralization are only complete at around 10 or 11 years of age, Newport adds.

The team worked with 39 children aged 4 through to 13, and 14 adults (aged 18-29). They were given a sentence comprehension task and researchers examined their patterns of brain activation as they worked. The fMRI data was recorded for each individual’s hemispheres separately and was then compared between four age groups: : 4-6, 7-9, 10-13, and 18-29. The team also carried out a whole-brain analysis for all participants to see which areas were activated during language comprehension across ages.

As an overall group, the team reports, even young children showed left lateralization of the process. However, a large number of them also showed heavy activation in the right hemisphere, which was not seen in adults. This area of the brain is involved in processing the emotional content of conversation in adults, the team notes.

Newport says that “higher levels of right hemisphere activation in a sentence processing task and the slow decline in this activation over development are reflections of changes in the neural distribution of language functions and not merely developmental changes in sentence comprehension strategies.”

The authors believe that younger children would show even greater involvement of their right hemisphere in comprehending speech. They plan to further their research by studying the same processes in teenagers and young adults who had a major left hemisphere stroke at birth.

The paper “The neural basis of language development: Changes in lateralization over age” has been published in the journal Proceedings of the National Academy of Sciences.

Pancreas adenocarcinoma.

This one gene seems to underpin pancreatic cancers in mice

Turning off one gene could completely block pancreatic cancer.

Pancreas adenocarcinoma.

Pancreas adenocarcinoma.
Image credits Ed Uthman / Flickr.

Pancreatic cells work in some pretty hazardous conditions. So, they come equipped with a particular gene that allows them to switch back to a more ‘primitive’ state and divide to make up for any fallen colleagues. However, this process can also create the conditions for pancreatic cancers to develop — and one group of researchers is looking into how to prevent it from happening. The results far exceeded their expectations.

Under maintenance

“We found that deleting the ATDC gene in pancreatic cells resulted in one of the most profound blocks of tumor formation ever observed in a well-known mice model engineered to develop pancreatic ductal adenocarcinoma, or PDA, which faithfully mimics the human disease,” says corresponding author Diane Simeone, MD, director of the Pancreatic Cancer Center of NYU Langone Health’s Perlmutter Cancer Center.

“We thought the deletion would slow cancer growth, not completely prevent it.”

The study built on the theory that pancreatic cancers develop when adult cells switch back to high-growth cell types (acinar-to-ductal metaplasia or ADM) — like those that drive fetal development — to repair local tissues. If this reversion takes place in the presence of genetic errors, the repair process quickly goes haywire, leading to unchecked cellular proliferation — cancer.

Led by researchers from the NYU School of Medicine and the University of Michigan, Ann Arbor, the team found that the ATDC gene must be active for injured pancreatic cells to undergo reversion. They focused on a type of pancreatic cells called acinar cells. Acinar cells produce enzymes to support digestion and dump them in the small intestine via a network of ducts.

But, they don’t call them digestive enzymes for nothing — these compounds do damage the ducts and associated cells as they move towards the small intestine. It’s not particularly heavy damage, but it does build up over time. As such, acinar cells have evolved to easily switch back into stem-like cell types, as did pancreatic duct cells, in order to heal this damage. If they do undergo this repair process after acquiring random DNA changes (mutations), however, they are prone to becoming cancerous. Mutations of a gene called KRAS, for example, have previously been linked to aggressive growth in more than 90% of pancreatic cancers, the team explains.

The team artificially caused pancreatitis in mice by treating them with cerulein, a signaling protein fragment that damages pancreatic tissue. ATDC gene expression (i.e. activation) did not increase right after the damage was caused. Rather, it took a few days to get going, which the team says is consistent with the timeframe required for acinar cells to reprogram genetically into their ductal cell forebears. Mutant KRAS and other genetic abnormalities induced aggressive pancreatic cancer in 100% of the mice used in the study — if the ATDC gene was present and active.

However, none of the mice used in the study developed pancreatic cancer in the absence of an active ATDC gene. Further experimentation has shown that ATDC gene expression triggers beta-catenin, a cell-signaling protein that activates another gene, SOX9. Previous research has linked SOX9 to the development of ductal stem cells and to the aggressive growth seen in PDA. The present study supports this link, finding that cells lacking ATDC can’t become cancerous due to their inability to induce SOX9 expression.

In human tissue, the team reports based on a study of 12 human pancreatic tissue samples, ATDC expression seems to be more pronounced than that seen in mice. Its activation increased further during the transition of ADM into human pancreatic ductal adenocarcinoma. The findings could help serve as a base for developing new prevention and treatment strategies for pancreatic cancer, the team concludes.

The paper “ATDC induces an invasive switch in KRAS-induced pancreatic tumorigenesis” has been published in the journal Genes & Development.