Broadly speaking: vocabulary in semantic dementia shifts towards general, semantically diverse words

One of the cardinal features of semantic dementia (SD) is a steady reduction in expressive vocabulary. We investigated the nature of this breakdown by assessing the psycholinguistic characteristics of words produced spontaneously by SD patients during an autobiographical memory interview. Speech was analysed with respect to frequency and imageability, and a recently-developed measure called semantic diversity. This measure quantifies the degree to which a word can be used in a broad range of different linguistic contexts. We used this measure in a formal exploration of the tendency for SD patients to replace specific terms with more vague and general words, on the assumption that more specific words are used in a more constrained set of contexts. Relative to healthy controls, patients were less likely to produce low-frequency, high-imageability words, and more likely to produce highly frequent, abstract words. These changes in the lexical-semantic landscape were related to semantic diversity: the highly frequent and abstract words most prevalent in the patients' speech were also the most semantically diverse. In fact, when the speech samples of healthy controls were artificially engineered such that low semantic diversity words (e.g., garage, spanner) were replaced with broader terms (e.g., place, thing), the characteristics of their speech production came to closely resemble that of SD patients. A similar simulation in which low-frequency words were replaced was less successful in replicating the patient data. These findings indicate systematic biases in the deterioration of lexical-semantic space in SD. As conceptual knowledge degrades, speech increasingly consists of general terms that can be applied in a broad range of linguistic contexts and convey less specific information.

Diverse mechanisms underlying the regulation of ion channels by carbon monoxide

Carbon monoxide (CO) is firmly established as an important, physiological signalling molecule as well as a potent toxin. Through its ability to bind metal-containing proteins, it is known to interfere with a number of intracellular signalling pathways, and such actions can account for its physiological and pathological effects. In particular, CO can modulate the intracellular production of reactive oxygen species, NO and cGMP levels, as well as regulate MAPK signalling. In this review, we consider ion channels as more recently discovered effectors of CO signalling. CO is now known to regulate a growing number of different ion channel types, and detailed studies of the underlying mechanisms of action are revealing unexpected findings. For example, there are clear areas of contention surrounding its ability to increase the activity of high conductance, Ca2+ -sensitive K+ channels. More recent studies have revealed the ability of CO to inhibit T-type Ca2+ channels and have unveiled a novel signalling pathway underlying tonic regulation of this channel. It is clear that the investigation of ion channels as effectors of CO signalling is in its infancy, and much more work is required to fully understand both the physiological and the toxic actions of this gas. Only then can its emerging use as a therapeutic tool be fully and safely exploited.

GANEing traction: the broad applicability of NE hotspots to diverse cognitive and arousal phenomena

GANE proposes that local glutamate-norepinephrine interactions enable “winner-take-more” effects in perception and memory under arousal. A diverse range of commentaries addressed both the nature of this ‘hotspot’ feedback mechanism and its implications in a variety of psychological domains, inspiring exciting avenues for future research.