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Category: neuroscience – Page 968

Cognitive training interventions are a promising approach to mitigate cognitive deficits common in aging and, ultimately, to improve functioning in older adults. Baseline neural factors, such as properties of brain networks, may predict training outcomes and can be used to improve the effectiveness of interventions. Here, we investigated the relationship between baseline brain network modularity, a measure of the segregation of brain sub-networks, and training-related gains in cognition in older adults. We found that older adults with more segregated brain sub-networks (i.e., more modular networks) at baseline exhibited greater training improvements in the ability to synthesize complex information. Further, the relationship between modularity and training-related gains was more pronounced in sub-networks mediating “associative” functions compared with those involved in sensory-motor processing. These results suggest that assessments of brain networks can be used as a biomarker to guide the implementation of cognitive interventions and improve outcomes across individuals. More broadly, these findings also suggest that properties of brain networks may capture individual differences in learning and neuroplasticity.

Trail Registration: ClinicalTrials.gov, NCT#00977418

Citation: Gallen CL, Baniqued PL, Chapman SB, Aslan S, Keebler M, Didehbani N, et al. (2016) Modular Brain Network Organization Predicts Response to Cognitive Training in Older Adults. PLoS ONE 11(12): e0169015. doi:10.1371/journal.pone.0169015

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Graphene has already proven its importance to brain implants as well as other Synbio technology.

Brain cell culture. Left: Normal astrocyte brain cell; Right: cancerous Glioblastoma Multiforme (GBM) version, imaged by Raman spectrography. (credit: B. Keisham et al./ACS Appl. Mater. Interfaces)

By interfacing brain cells with graphene, University of Illinois at Chicago researchers have differentiated a single hyperactive Glioblastoma Multiforme cancerous astrocyte cell from a normal cell in the lab — pointing the way to developing a simple, noninvasive tool for early cancer diagnosis.

In the study, reported in the journal ACS Applied Materials & Interfaces, the researchers looked at lab-cultured human brain astrocyte cells taken from a mouse model. They compared normal astrocytes to their cancerous counterpart, highly malignant brain tumor glioblastoma multiforme.

Continue reading “Using graphene to detect brain cancer cells” | >

Rejuvenating the immune system offers hope for Alzheimer’s patients and removal of plaques.

Alzheimer′s disease (AD) is characterized by deposition of amyloid plaques, neurofibrillary tangles, and neuroinflammation. In order to study microglial contribution to amyloid plaque phagocytosis, we developed a novel ex vivo model by co‐culturing organotypic brain slices from up to 20‐month‐old, amyloid‐bearing AD mouse model (APPPS1) and young, neonatal wild‐type (WT) mice. Surprisingly, co‐culturing resulted in proliferation, recruitment, and clustering of old microglial cells around amyloid plaques and clearance of the plaque halo. Depletion of either old or young microglial cells prevented amyloid plaque clearance, indicating a synergistic effect of both populations. Exposing old microglial cells to conditioned media of young microglia or addition of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) was sufficient to induce microglial proliferation and reduce amyloid plaque size. Our data suggest that microglial dysfunction in AD may be reversible and their phagocytic ability can be modulated to limit amyloid accumulation. This novel ex vivo model provides a valuable system for identification, screening, and testing of compounds aimed to therapeutically reinforce microglial phagocytosis.

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It may be possible to reduce, stop or even prevent absence seizures, the most common form of childhood epilepsy, according to a study published in the leading scientific journal Neuron.

Using an advanced technology called optogenetics and a rodent model, researchers at Stanford University School of Medicine showed that it is possible to trigger seizures by inducing synchronized, rhythmic activity within a particular structure in the brain called the thalamocortical tract. Importantly, they also demonstrated that disrupting this activity is sufficient to terminate the seizures.

For the study the team, led by Dr Jeanne Paz, inserted a gene that encodes for a light-sensitive cell-surface protein into a set of nerve cells situated in the thalamocortical tract of rat and mice models of absence seizures. This way, the scientists were able to prevent these cells from firing by shining a yellow light onto them.

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A new genetic disease has been discovered that could play a key role in devastating brain conditions such as Alzheimer’s and Parkinson’s, opening up the possibility of new forms of treatment.

A 47-year-old Canadian woman, who had been having difficulty walking and balancing since she was 28, was found to have a new genetic disease after 10 known conditions were ruled out, according to a paper in the journal Nature by an international team of researchers.

The disease causes an over-reaction by the body’s natural repair system. An enzyme, known as PARP1, goes into over-drive, ultimately causing the deaths of brain cells.

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A new biomarker for Alzheimers could improve the patient outcome and allow for earlier treatment.

An enzyme found in the fluid around the brain and spine is giving researchers a snapshot of what happens inside the minds of Alzheimer’s patients and how that relates to cognitive decline.

Iowa State University researchers say of the enzyme, autotaxin, significantly predict impairment and Type 2 diabetes. Just a one-point difference in autotaxin levels — for example, going from a level of two to a three — is equal to a 3.5 to 5 times increase in the odds of being diagnosed with some form of memory loss, said Auriel Willette, an assistant professor of food science and human nutrition at Iowa State.

Autotaxin, often studied in cancer research, is an even stronger indicator of Type 2 diabetes. A single point increase reflects a 300 percent greater likelihood of having the disease or pre-diabetes. The results are published in the Journal of Alzheimer’s Disease. Willette and Kelsey McLimans, a graduate research assistant, say the discovery is important because of autotaxin’s proximity to the .

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More progress on the cancer front! Controlling cancer effectively is a critical part of rejuvenation biotechnology and therefore all cancer progress is of great interest to our community. If there was a poster child of aging diseases, cancer would be at the front of the queue.

“The results could lead to new treatments—not only for a variety of cancers, but also other diseases that arise from faulty proteinases, such as Alzheimer’s, asthma, multiple sclerosis and arthritis.”

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Scientists are able to use brain tests on three-year-olds to determine which children are more likely to grow up to become criminals. It sounds like Minority Report come to life: An uncomfortable idea presenting myriad ethical concerns. But, though unnerving, the research is nuanced and could potentially be put to good use.

In the study, published in Nature Human Behavior this week, researchers led by neuroscientists at Duke University showed that those with the lowest 20% brain health results aged three went on to commit more than 80% of crimes as adults. The research used data from a New Zealand longitudinal study of more than 1,000 people from birth in the early 1970s until they reached 38 years old. This distribution, of 20% of a population accounting for 80% of an effect, is strong but not unusual. In fact, it follows the “Pareto principle.” The authors write in their paper:

In Pareto’s day, the problem definition was that 20% of families owned 80% of land in Italy. The so-called Pareto principle is alive and useful today: for example, in software engineering, 20% of the code is said to contain 80% of the errors.

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What combinations of mutations help cancer cells survive? Which cells in the brain are involved in the onset of Alzheimer’s? How do immune cells conduct their convoluted decision-making processes? Researchers at the Weizmann Institute of Science have now combined two powerful research tools — CRISPR gene editing and single cell genomic profiling — in a method that may finally help us get answers to these questions and many more.

The new technology enables researchers to manipulate gene functions within single cells, and understand the results of each change in extremely high resolution. A single experiment with this method, say the scientists, may be equal to thousands of experiments conducted using previous approaches, and it may advance the field of genetic engineering for medical applications.

The gene-editing technique CRISPR is already transforming biology research around the world, and its clinical use in humans is just around the corner. CRISPR was first discovered in bacteria as a primitive acquired immune system, which cuts and pastes viral DNA into their own genomes to fight viruses. In recent years, this bacterial system has been adopted by researchers to snip out or insert nearly any gene in any organism or cell, quickly and efficiently. “But CRISPR, on its own, is a blunt research tool, since we often have trouble observing or understanding the outcome of this genomic editing,” says Prof. Ido Amit of the Weizmann Institute of Science’s Immunology Department, who led the study. “Most studies so far have looked for black-or-white types of effects,” adds Dr. Diego Jaitin, of Amit’s lab group, “but the majority of processes in the body are complex and even chaotic.”

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