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Polyglutamine expansion in the androgen receptor, causing X-linked spinal and bulbar muscular atrophy, impairs its function as a transcriptional coactivator regulating an extensive network of proteins involved in protein clearance.
In this issue, Shenhav et al. critically evaluate the idea that neural correlates of value actually represent value. They describe how, in many situations, value correlates can reflect other cognitive factors, such as decisional difficulty.
Two independent epigenome-wide association studies of Alzheimer's disease cohorts have identified overlapping methylation signals in four loci, ANK1, RPL13, RHBDF2 and CDH23, not previously associated with Alzheimer's disease. These studies also suggest that epigenetic changes contribute more to Alzheimer's disease than expected.
Molecular orchestration mediated by Fezf2, a master transcriptional regulator of a particular type of cortical neurons, directly determines both their identity and axonal routing, and thus their connectivity.
Brain–machine interfaces provide not only potential therapies, but also new tools for studying neuronal processing. A study now uses them to investigate how learning affects sleep activity in motor cortex.
Does cell-to-cell spreading of misfolded proteins occur in all neurodegenerative disorders? A study in this issue of Nature Neuroscience now demonstrates propagation of mutant huntingtin in brain slice cultures and in vivo, thereby extending the process of cell-to-cell propagation of misfolded proteins to Huntington's disease.
The orbitofrontal cortex and ventral striatum encode expected outcomes during economic decision-making. Research now demonstrates that activity in these structures also represents missed opportunities during a foraging task cleverly designed to elicit regret in rats, the Restaurant Row task.
A report reveals that giant subcortical heterotopia is caused by mutation of a microtubule-associated protein, Eml1. Defects in Eml1 lead to disruption of the radial migratory scaffolding network in mice and humans.
The proliferation of NSCs in the adult SVZ is controlled by a set of neurons expressing choline acetyltransferase, identifying a mechanism connecting brain activity to neurogenesis in the adult mammalian brain.
A leading therapeutic molecule for multiple sclerosis, FTY720, is shown to mimic a key component of sphingolipid signaling, resulting in specific manipulation of histone deacetylases and the extinction of memory.
A study now shows that variability in neuronal responses in the visual system mainly arises from slow fluctuations in excitability, presumably caused by factors of nonsensory origin, such as arousal, attention or anesthesia.
We now learn that mutant huntingtin binds to a complex that imports constituent proteins across the mitochondrial inner membrane, halting bioenergetics in synaptic mitochondria and predisposing to neuronal dysfunction and death.
Spike-based approaches to feature selectivity in sensory pathways can bias toward only the most active neurons. A subthreshold method identifies feature selectivity in the rodent vibrissal system regardless of spiking activity.
Brain-computer interfaces (BCIs) and optical imaging have both undergone impressive technological growth in recent years. A study in which mice learn to modulate neural activity merges these technologies to investigate the neural basis of BCI learning with unprecedented spatial detail.
Stimulating the brain in the gamma frequency range, which is the frequency band most often associated with conscious awareness in the awake state, boosts the ability to engage in lucid dreaming during REM sleep.
Grid cells have been proposed to reflect competitive interactions in inhibitory neural networks. Experimental results obtained using optogenetics to identify spikes emitted specifically by parvalbumin interneurons now constrain the mechanisms by which such networks could give rise to grid cells.
It is widely believed that Huntington's disease is driven exclusively by neuronal dysfunction. Work now challenges this view, showing that mutant huntingtin in astrocytes leads to dysregulation of extracellular K+.
