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Monday, January 23, 2012

Brain scans spot early signs of dyslexia

By Julie Steenhuysen

Reuters

Monday, January 23, 2012

CHICAGO (Reuters) - Instead of waiting for a child to experience reading delays, scientists now say they can identify the reading problem even before children start school, long before they become labeled as poor students and begin to lose confidence in themselves.

Although typically diagnosed during the second or third grade of school - around age 7 or 8 - a team from Children's Hospital Boston said they could see signs of the disease on brain scans in children as early as 4 and 5, a time when studies show children are best able to respond to interventions.

"We call it the dyslexia paradox," said Nadine Gaab of the Laboratories of Cognitive Neuroscience at Children's, whose study was published in Proceedings of the National Academy of Sciences.

Gaab said most children are not diagnosed until third grade, but interventions work best in younger children, hopefully before they begin to learn to read.

"Often, by the time they get a diagnosis, they usually have experienced three years of peers telling them they are stupid, parents telling them they are lazy. We know they have reduced self esteem. They are really struggling," Gaab said in a telephone interview.

Her study builds on an emerging understanding of dyslexia as a problem with recognizing and manipulating the individual sounds that form language, which is known as phonological processing.

In order to read, children must map the sounds of spoken language onto specific letters that make up words. Children with dyslexia struggle with this mapping process.

"The beauty is spoken language can present before written language so people can look for symptoms," said Dr. Sally Shaywitz, a director of the Center for Dyslexia and Creativity at Yale University.

Signs of early dyslexia might include difficulty with rhyming, mispronouncing words or confusing similar-sounding words.

"Those are all very early symptoms," Shaywitz said.

Dyslexia affects roughly 5 percent to 17 percent of all children and up to 1 in 2 children with a family history of the disorder will struggle with reading, have poor spelling and experience difficulty decoding words.

In her study, Gaab and colleagues scanned the brains of 36 preschool children while they did a number of tasks, such as trying to decide if two words start with the same sound.

They found that during these tasks, children who had a family history of dyslexia had less brain activity in certain regions of the brain than did children of similar ages, intelligence and socioeconomic status.

Older children and adults with dyslexia have dysfunction in these same areas of the brain, which include the junctions between the occipital and temporal lobes and the temporal and parietal lobes in the back of the brain.

Gaab said the study shows that when children predisposed to dyslexia did these tasks, their brains did not use the area typically used for processing this information. This problem occurred even before the children started learning to read.

"The important point of this paper is it shows the need to look for signs of dyslexia earlier," said April Benasich, director of the Carter Center for Neurocognitive Research at Rutgers, the State University of New Jersey, who was not part of the study.

Benasich studies language processing in even younger children - babies who have a family history of learning disorders.

"There is evidence to suggest that what is thought to be reading failure is there before the kids fail," she said.

Gaab said her study is too small to form the basis of any test for dyslexia but her team has just won a grant from the National Institutes of Health to do a larger study.

Ultimately, she hopes parents will be able to go to their pediatrician and ask for their child to be assessed.

"Families often know that their child has dyslexia as early as kindergarten, but they can't get interventions at their schools," she said in a statement.

"If we can show that we can identify these kids early, schools may be encouraged to develop programs," she said.

(Editing by Bill Trott)

Patterns of Chromosome Abnormality: The Key to Cancer?

ScienceDaily

Monday, January 23, 2012

ScienceDaily (Jan. 23, 2012) — A healthy genome is characterized by 23 pairs of chromosomes, and even a small change in this structure -- such as an extra copy of a single chromosome -- can lead to severe physical impairment. So it's no surprise that when it comes to cancer, chromosomal structure is frequently a contributing factor, says Prof. Ron Shamir of the Blavatnik School of Computer Science at Tel Aviv University.

Now Prof. Shamir and his former doctoral students Michal Ozery-Flato and Chaim Linhart, along with fellow researchers Prof. Shai Izraeli and Dr. Luba Trakhtenbrot from the Sheba Medical Center, have combined techniques from computer science and statistics to discover that many chromosomal pairs are lost or gained together across various cancer types. Moreover, the researchers discovered a new commonality of chromosomal aberrations among embryonic cancer types, such as kidney, skeleton, and liver cancers.

These findings, recently published in Genome Biology, could reveal more about the nature of cancer. As cancer develops, the genome becomes increasingly mutated -- and identifying the pattern of mutation can help us to understand the nature and the progression of many different kinds of cancer, says Prof. Shamir.

Looking at the big picture

As cancer progresses, the structure of chromosomes is rearranged, individual chromosomes are duplicated or lost, and the genome becomes abnormal. Some forms of cancer can even be diagnosed by identifying individual chromosomal aberrations, notes Prof. Shamir, pointing to the example of a specific type of leukemia that is caused by small piece of chromosome 9 being moved to chromosome 22.

When analyzing many different kinds of cancer, however, the researchers discovered that chromosomal aberrations among different cancers happen together in a noticeable and significant way. The researchers studied a collection of more than fifty thousand cancer karyotypes -- representations of chromosomal layouts in a single cell -- and charted them according to commonalities. The researchers were not only able to confirm different chromosomal aberrations that appeared in specific cancer types, but also for the first time identified a broader effect of pairs of chromosomes being lost or gained together across different cancer types.

It was also the first time that researchers saw a connection among solid kidney, skeleton, and liver cancers. While it was known that these cancers all develop in the embryo, they were previously analyzed independently. The TAU researchers have now confirmed that they share chromosomal characteristics and aberrations, much like various forms of leukemia or lymphomas.

Aberrations a driving force for cancer

Under normal circumstances, even a small change to a person's chromosomal structure can be devastating. For example, Down's syndrome is caused by a single extra copy of Chromosome 21. "But in cancer, there are many cases of extra or missing chromosomes. Yet cancer cells thrive more effectively than other cells," Prof. Shamir says.

Prof. Shamir hopes that future investigation into these chromosomal aberrations will give researchers more clues into why something that is so detrimental to our healthy development is so beneficial to this disease. Cancer is the result of sequences of events, he says, each causing the genome to become more mutated, mixed, and duplicated. Tracking these changes could aid our understanding of the driving forces of cancer's progress.

Prof. Shamir heads the Edmond J. Safra Program for Bioinformatics and holds the Raymond and Beverly Sackler Chair in Bioinformatics.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Story Source:

The above story is reprinted from materials provided by American Friends of Tel Aviv University.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Michal Ozery-Flato, Chaim Linhart, Luba Trakhtenbrot, Shai Izraeli, Ron Shamir. Large-scale analysis of chromosomal aberrations in cancer karyotypes reveals two distinct paths to aneuploidy. Genome Biology, 2011; 12 (6): R61 DOI: 10.1186/gb-2011-12-6-r61

Keeping brain sharp may ward off Alzheimer's protein

By Julie Steenhuysen

Reuters

Monday, January 23, 2012

CHICAGO (Reuters) - People who challenge their brains throughout their lifetimes -- through reading, writing and playing games -- are less likely to develop protein deposits in the brain linked with Alzheimer's, U.S. researchers said on Monday.

Prior studies have suggested that people who are well educated and stay mentally active build up brain reserves that allow them to stay sharp even if deposits of the destructive protein called beta amyloid form in the brain.

But the latest study, based on brain-imaging research, suggests that people who stay mentally engaged beginning in childhood and remain so throughout their lives actually develop fewer amyloid plaques.

"We're not talking about the brain's response to amyloid. We're talking about the actual accumulation of amyloid," Dr. William Jagust of the University of California, Berkeley, whose study appears in the Archives of Neurology, said in an interview. "It's a brand new finding."

While small, the study also shows that starting brain-stimulating activities early enough might offer a way to prevent Alzheimer's-related plaques from building up in the brain.

Currently, there are no drugs that can prevent Alzheimer's disease, which scientists now think begins 10 to 15 years before memory problems set in.

Alzheimer's Disease International estimates there are now 36 million people with the disease worldwide. As the population ages, that number will increase to 66 million by 2030, and to 115 million by 2050.

Last week, the U.S. government released draft recommendations for a national Alzheimer's plan that calls for finding effective treatments or prevention strategies by 2025.

The new study involved the use of an imaging agent known as Pittsburgh Compound B or PiB, which works with positron emission tomography, or PET scanners. This chemical sticks to and highlights deposits of beta amyloid.

"Beta amyloid is the protein that many people feel may be the initiating factor in Alzheimer's disease. It is the protein that is in the plaques of the brains of people with Alzheimer's," Jagust said.

Starting  Crossword Puzzles Late Won’t  Help

The researchers studied 65 healthy, cognitively normal people aged 60 and older. Study participants were asked a battery of questions about how mentally active they had been during different periods of their lives starting at age 6. The questions included whether they had read newspapers, went to the library, wrote letters or e-mails and played games.

They also underwent extensive testing to assess their memory and thinking skills and their brains were scanned using the new tracer to look for amyloid deposits in the brain.

The team compared the brain scans with those of 10 Alzheimer's patients and 11 healthy people in their 20s.

They found that people who had been the most mentally active had lower levels of beta amyloid than others who had been less mentally active.

People in the study who had recently taken up crosswords and other mental exercises did not appear to see much benefit.

"What our data suggests is that a whole lifetime of engaging in these activities has a bigger effect than being cognitively active just in older age," said Susan Landau, another Berkeley researcher who worked on the study.

She said amyloid probably starts accumulating many years before symptoms appear, so by the time memory problems start, there is little that can be done. "The time for intervention may be much sooner," she said in a statement.

One weakness is that the study relies on people's memory of their mental activities, Jagust said.

He said staying mentally engaged may make the brain more efficient, which could have a protective effect, but that is still not clear.

(Reporting by Julie Steenhuysen; Editing by Michele Gershberg and Sandra Maler)

Sunday, January 22, 2012

Plant Flavonoid Luteolin Blocks Cell Signaling Pathways in Colon Cancer Cells

ScienceDaily

Sunday, January 22, 2012

ScienceDaily (Jan. 22, 2012) — Luteolin is a flavonoid commonly found in fruit and vegetables. This compound has been shown in laboratory conditions to have anti-inflammatory, anti-oxidant and anti-cancer properties but results from epidemiological studies have been less certain. New research published in BioMed Central's open access journal BMC Gastroenterology shows that luteolin is able to inhibit the activity of cell signaling pathways (IGF and PI3K) important for the growth of cancer in colon cancer cells.

Colon cancer is the second most frequent cause of cancer-related death in the Western World. Colon cancer cells have elevated levels of IGF-II compared to normal colon tissues. It is thought that this is part of the mechanism driving uncontrolled cell division and cancer growth. Researchers from Korea showed that luteolin was able to block the secretion of IGF-II by colon cancer cells and within two hours decreased the amount of receptor (IGF-IR) precursor protein. Luteolin also reduced the amount of active receptor (measured by IGF-I dependent phosphorylation).

Luteolin inhibited the growth stimulatory effect of IGF-I and the team led by Prof Jung Han Yoon Park found that luteolin affected cell signaling pathways which are activated by IGF-I in cancer. Prof Jung Han Yoon Park explained, "Luteolin reduced IGF-I-dependent activation of the cell signaling pathways PI3K, Akt, and ERK1/2 and CDC25c. Blocking these pathways stops cancer cells from dividing and leads to cell death."

Prof Jung Park continued, "Our study, showing that luteolin interferes with cell signaling in colon cancer cells, is a step forward in understanding how this flavonoid works. A fuller understanding of the in vivo results is essential to determine how it might be developed into an effective chemopreventive agent."

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Story Source:

The above story is reprinted from materials provided by BioMed Central Limited, via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Do Young Lim, Han Jin Cho, Jongdai Kim, Chu Won Nho, Ki Won Lee and Jung Han Yoon Park. Luteolin decreases IGF-II production and downregulates insulin-like growth factor-I receptor signaling in HT-29 human colon cancer cells. BMC Gastroenterology, 2012 [link]