***********NATURE NEUROSCIENCE *****************
(http://www.nature.com/natureneuroscience)
[1] A noisy basis for dyslexia
DOI: 10.1038/nn1474
Children with dyslexia have trouble processing the sounds that make up words, but the underlying cause of this problem is controversial. Dyslexic children are much worse than non-dyslexic children at seeing visual signals through noise, reports a paper in the July issue of Nature Neuroscience, which may explain the origin of the reading problem.
Anne Sperling and colleagues asked dyslexic and non-dyslexic children to detect a pattern embedded in visual 'noise'�, which looks like the static on a television screen. Compared to the non-dyslexic children, dyslexic children needed the pattern to be much brighter before they could see it. This finding contradicts a popular idea in the field, which attributes impaired visual processing in dyslexics to defects in a subset of visual neurons known as the magnocellular pathway. The authors now separate the effect of noise from the effect of the pathway, and conclude that deficits in noise exclusion can explain those previous findings.
How might a problem with noise exclusion interfere with learning to read? The authors suggest that it may interfere with letter recognition, or that the problem of distinguishing signal from noise might extend to other senses, including the auditory system.
Author contact:
Anne Sperling (Georgetown University Medical Center, Washington, DC, USA)
Tel: +1 202 687 1767; E-mail: [email protected]
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[2] Dominant role of the GluR2 subunit in regulation of AMPA receptors by CaMKII
DOI: 10.1038/nn1476
[3] Nonclassical, distinct endocytic signals dictate constitutive and PKC-regulated neurotransmitter transporter internalization
DOI: 10.1038/nn1478
[4] In vivo auditory brain mapping in mice with Mn-enhanced MRI
DOI: 10.1038/nn1477
*************************************NATURE CHEMICAL BIOLOGY ***********************************
(http://www.nature.com/nchembio)
[5] A new path to cell death
DOI: 10.1038/nchembio711
A new pathway to necrosis, a form of cell death, is described in July's Nature Chemical Biology. Necrosis is a common feature of human pathologies from stroke to neurodegeneration and unlike apoptosis -- a precisely orchestrated cellular pathway to initiate death -- was generally believed to be a passive cellular response to external damage. Junying Yuan and colleagues identify a previously unknown cellular pathway leading to necrosis, which they call necroptosis. The team demonstrate its involvement in conditions where not enough blood reaches the brain, otherwise known as ischemic brain injury.
A growing number of studies have reported evidence for non-apoptotic cell death with some features of necrosis. However, scientists have had no tools to investigate the potential mechanisms behind these observations. To address this, Yuan and colleagues identified a chemical, necrostatin-1, which specifically inhibited this non-apoptotic cell death. They found that necrostatin-1 blocked all cases of this cell death, demonstrating the existence of a specific cellular pathway, necroptosis, leading to necrosis. They further showed that necrostatin-1 reduced ischemic brain injury in a mouse model of stroke, establishing a causal role of necroptosis in ischemic trauma induced neuronal damage. Necrostatin-1 is a promising therapeutic lead for treating patients with brain injury following stroke.
In addition to its therapeutic potential, necrostatin-1 provides an important new chemical tool for investigating the precise molecular mechanism of necroptosis and the role of this pathway in other pathologies involving necrosis.
Author contact:
Junying Yuan (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 432 4170, E-mail: [email protected]
Additional contact for comment on paper:
David Wallach (Weizmann Institute, Rehovot, Israel)
Tel: +972 8 934 3941, E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE (http://www.nature.com/nature)
[6] Trans-SNARE pairing can precede a hemifusion intermediate in intracellular membrane fusion
DOI: 10.1038/nature03722
NATURE MEDICINE (http://www.nature.com/naturemedicine)
[7] A new approach to an influenza live vaccine: modification of the cleavage site of the hemagglutinin
DOI: 10.1038/nm1256
[8] Lack of the architectural transcription factor HMGA1 causes severe insulin resistance and diabetes in humans and mice
DOI: 10.1038/nm1254
NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnolgy)
[9] Rapid generation of specific antibodies by enhanced homologous recombination
DOI: 10.1038/nbt1092
NATURE GENETICS (http://www.nature.com/naturegenetics)
[10] Temporal dissection of p53 function in vitro and in vivo
DOI: 10.1038/ng1572
[11] Gains of glycosylation comprise an unexpectedly large group of pathogenic mutations
DOI: 10.1038/ng1581
[12] Atypical RNA polymerase subunits required for RNA-directed DNA methylation
DOI: 10.1038/ng1580
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[13] Inhibitors of gamma-secretase block in vivo and in vitro T helper type 1 polarization by preventing Notch upregulation of Tbx21
DOI: 10.1038/ni1209
[14] Stable T cell dendritic cell interactions precede the development of both tolerance and immunity in vivo
DOI: 10.1038/ni1210
[15] Suppressor of cytokine signaling 1 is required for the accurate differentiation of CD4+ T cells
DOI: 10.1038/ni1211
[16] A plague of autoantibodies
DOI: 10.1038/ni1214
