498 Deletions of chromosome 22q13.3 cause Phelan–McDermid syndrome (PMDS), a neurodevelopmental disorder associated with autism; here induced pluripotent stem cells from PMDS patients with autism are used to produce neurons, they are shown to have reduced SHANK3 expression and a defect in excitatory synaptic transmission which can be restored either by increasing SHANK3 or with insulin-like growth factor 1.
http://www.nature.com/nature/journal/v503/n7475/full/nature12618.html
497 High-speed laser microsurgery of alert fruit flies for fluorescence imaging of neural activity.
http://www.pnas.org/content/110/46/18374.abstract
496 Human genome–guided identification of memory-modulating drugs.
http://www.pnas.org/content/110/46/E4369.abstract
495 Chondroitin sulphate N-acetylgalactosaminyl-transferase-1 inhibits recovery from neural injury.
http://www.nature.com/ncomms/2013/131112/ncomms3740/full/ncomms3740.html
494 A cholinergic trigger drives learning-induced plasticity at hippocampal synapses.
http://www.nature.com/ncomms/2013/131112/ncomms3760/full/ncomms3760.html
493 Soluble forms of polyQ-expanded huntingtin rather than large aggregates cause endoplasmic reticulum stress.
http://www.nature.com/ncomms/2013/131112/ncomms3753/full/ncomms3753.html
492 Reducing cannabinoid abuse and preventing relapse by enhancing endogenous brain levels of kynurenic acid .
http://www.nature.com/neuro/journal/v16/n11/abs/nn.3540.html
491 There is currently no effective treatment for infantile neuronal ceroid lipofuscinosis, a neurodegenerative lysosomal storage disease that occurs in childhood. Here the authors show that a small molecule thioesterase-mimetic can alleviate neuropathology and extend lifespan in an animal model of the disease.
http://www.nature.com/neuro/journal/v16/n11/abs/nn.3526.html
490 Dysfunction of the potassium-chloride cotransporter KCC2 has been linked to many neurological diseases, including pain, anxiety and epilepsy. Now, Yves De Koninck and his colleagues report that they have developed a novel small-molecule compound that is orally bioavailable and can activate KCC2 and reduce chronic pain in rats.
http://www.nature.com/nm/journal/v19/n11/abs/nm.3356.html
489 Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by loss of the translational repressor protein FMRP. Now, Joel D. Richter and his colleagues report that knocking down the expression of the translational activator protein CPEB can restore normal levels of translation and rescue behavioral deficits in a mouse model of FXS.
http://www.nature.com/nm/journal/v19/n11/abs/nm.3353.html
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