Women who take prenatal vitamins and eat cereal supplemented with folic acid in the early months of pregnancy are less likely to have children with autism compared with women who consume less folate, suggests preliminary data from a survey presented today at the Society for Neuroscience conference.
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Treatment with the insulin-like growth factor (IGF) greatly improves the health of mouse models of Rett syndrome ― a regressive genetic disorder that causes mental retardation, seizures and features of autism ― according to unpublished researched presented this morning at the Society for Neuroscience conference.
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The formation of new neurons ― or neurogenesis ― is an intricate process that occurs in both developing and adult brains. Neural stem cells first give rise to round nerve cell bodies, which then form long and skinny nerve projections through various layers of the cortex and synaptic connections to larger other networks of neurons.
Studying brain cells in culture, neuroscientist Guo-li Ming from Johns Hopkins University compared the entire process of neurogenesis in the hippocampus of normal mice and in mice with reduced expression of DISC1, a gene that has been strongly associated with schizophrenia.
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Brain tissue from individuals with autism is rare, to say the least: of the 30,000 samples in the National Institutes of Healthʼs Brain and Tissue Bank for Developmental Disorders, for instance, only 30 are from individuals diagnosed with autism.
The tissue bank has sent samples to 45 researchers thus far including, notably, Eric Courchesne. But according to Ronald Zielke, who has directed the bank since its creation in 1991, up to 20% of the tissues they distribute are used in some kind of research on autism.
Here, at the Society for Neuroscience annual meeting, Zielke explains to Virginia Hughes how brain banks collect samples for autism research, and how they make the difficult decisions to distribute them for research.
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A new technique, optogenetics, makes it possible to study both the micro and the macro levels of brain activity.
The technique allows scientists to stimulate activity in specific types of neurons with light, rather than with invasive metal electrodes.
Stanford University bioengineer Karl Deisseroth, who has used optogenetics in live mouse models since 2007, described the technique to a packed room of about 50 scientists this morning at the Society for Neuroscience conference.
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A mouse model of neurofibromatosis ― a genetic neurodevelopmental disorder that leads to nerve tumors, memory problems and, often, autism ― exhibits deficits in social interaction and social learning, according to research presented in a poster session today at the Society for Neuroscience conference.
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In the wake of a bribery scandal and a disastrous baby formula recall, Chinese leaders are carrying out a slew of healthcare reforms.
In mid-October, in part on the basis of recommendations from the World Health Organization and the World Bank, China’s State Council published a proposal for healthcare reform online for one month of public comment. Part of the proposal states that by 2020, all Chinese citizens will be covered under one of three different government health insurance schemes. Currently, an estimated 35% of urban households and 43% of rural households cannot afford healthcare.
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Nearly one out of every ten couples worldwide cannot conceive a child after trying for a year, according to recent epidemiological studies. The cause remains unknown among 25% of those with infertility. Now, new genetic studies suggest that, in some cases, the culprit might, in fact, lie hidden in one’s DNA.
So far, scientists have identified nearly 300 DNA mutations in men with reproductive defects. When modeled in mice, many of these mutations have a pivotal role in the development of the ovaries, testes and especially sperm. Sperm and egg development starts with meiosis, a process in which chromosomes line up before self-segregating into daughter cells. During this process, pairs of chromosomes carry out an intricate cellular choreography of migrations and alignments to effectively swap genetic information.
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Just after dusk on April 12, silence fell over the crowd of Seton Hall students, faculty and alumni who gathered at the Richard and Sheila Regan Fieldhouse. A bagpiper began a slow, melancholy rendition of “Amazing Grace,” while a large-screen projector displayed the names of people who had succumbed to cancer. More than 500 white luminaria lined the track, one for each of the dead.
This luminaria ceremony — probably the most emotional part of Seton Hall’s “Relay for Life” fundraiser for the American Cancer Society (ACS) — would never have been possible without the dogged perseverance of junior Michael Jacobson, 20. Jacobson, who has a genetic predisposition to cancer, was committed to founding a Relay program here from the moment he stepped on campus.
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