Recent electrophysiological investigations of the auditory system in primates along with functional neuroimaging studies of auditory perception in humans have suggested there are two pathways arising from the primary auditory cortex. In the primate brain, a 'ventral' pathway is thought to project anteriorly from the primary auditory cortex to prefrontal areas along the superior temporal gyrus while a separate 'dorsal' route connects these areas posteriorly via the inferior parietal lobe. We use diffusion MRI tractography, a noninvasive technique based on diffusion-weighted MRI, to investigate the possibility of a similar pattern of connectivity in the human brain for the first time. The dorsal pathway from Wernicke's area to Broca's area is shown to include the arcuate fasciculus and connectivity to Brodmann area 40, lateral superior temporal gyrus (LSTG), and lateral middle temporal gyrus. A ventral route between Wernicke's area and Broca's area is demonstrated that connects via the external capsule/uncinate fasciculus and the medial superior temporal gyrus. Ventral connections are also observed in the lateral superior and middle temporal gyri. The connections are stronger in the dominant hemisphere, in agreement with previous studies of functional lateralization of auditory-language processing.

Alzheimer's disease impairs long term memories for related events (e.g. faces with names) more than for single events (e.g. list of faces or names). Whether or not this associative or 'binding' deficit is also found in short-term memory has not yet been explored. In two experiments we investigated binding deficits in verbal short-term memory in Alzheimer's disease. Experiment 1: 23 patients with Alzheimer's disease and 23 age and education matched healthy elderly were recruited. Participants studied visual arrays of objects (six for healthy elderly and four for Alzheimer's disease patients), colours (six for healthy elderly and four for Alzheimer's disease patients), unbound objects and colours (three for healthy elderly and two for Alzheimer's disease patients in each of the two categories), or objects bound with colours (three for healthy elderly and two for Alzheimer's disease patients). They were then asked to recall the items verbally. The memory of patients with Alzheimer's disease for objects bound with colours was significantly worse than for single or unbound features whereas healthy elderly's memory for bound and unbound features did not differ. Experiment 2: 21 Alzheimer's disease patients and 20 matched healthy elderly were recruited. Memory load was increased for the healthy elderly group to eight items in the conditions assessing memory for single or unbound features and to four items in the condition assessing memory for the binding of these features. For Alzheimer's disease patients the task remained the same. This manipulation permitted the performance to be equated across groups in the conditions assessing memory for single or unbound features. The impairment in Alzheimer's disease patients in recalling bound objects reported in Experiment 1 was replicated. The binding cost was greater than that observed in the healthy elderly group, who did not differ in their performance for bound and unbound features. Alzheimer's disease grossly impairs the mechanisms responsible for holding integrated objects in verbal short-term memory.

Performance on tests of odour discrimination, naming, and matching was compared in patients with four distinct forms of neurodegenerative disease: Alzheimer's disease (AD), semantic dementia (SD), frontotemporal dementia (FTD), and corticobasal degeneration (CBD). The SD patients were found to have a severe impairment of identification from olfaction despite having normal discrimination, consistent with the multimodal semantic impairment characteristic of this patient group. The AD patients' poor odour discrimination suggests that a perceptual impairment is the root of their poor odour identification. Mild impairments in odour identification observed in FTD and CBD are consistent with their generalised executive dysfunction. The findings illustrate that breakdown in olfaction can occur at a perceptual or semantic level, analogous to the distinction between apperceptive and associative forms of deficit in the visual and auditory modalities. The findings add further insights into the nature of the semantic deficit in SD by exploring a hitherto neglected modality and may have relevance in explaining the altered eating habits commonly associated with SD.

Binding is a cognitive function responsible for integrating features within complex stimuli (e.g., shape-colour conjunctions) or events within complex memories (e.g., face-name associations). This function operates both in short-term memory (STM) and in long-term memory (LTM) and is severely affected by Alzheimer's disease (AD). However, forming conjunctions in STM is the only binding function which is not affected by healthy ageing or chronic depression. Whether this specificity holds true across other non-AD dementias is as yet unknown. The present study investigated STM conjunctive binding in a sample of AD patients and patients with other non-AD dementias using a task which has proved sensitive to the effects of AD. The STM task assesses the free recall of objects, colours, and the bindings of objects and colours. Patients with AD, frontotemporal dementia, vascular dementia, lewy body dementia and dementia associated with Parkinson's disease showed memory, visuo-spatial, executive and attentional deficits on standard neuropsychological assessment. However, only AD patients showed STM binding deficits. This deficit was observed even when memory for single features was at a similar level across patient groups. Regression and discriminant analyses confirmed that the STM binding task accounted for the largest proportion of variance between AD and non-AD groups and held the greatest classification power to identify patients with AD. STM conjunctive binding places little demands on executive functions and appears to be subserved by components of the memory network which are targeted by AD, but not by non-AD dementias.