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James C.,University of Western Sydney | Macefield V.G.,University of Western Sydney | Macefield V.G.,Prince of Wales Medical Research Institute
Autonomic Neuroscience: Basic and Clinical | Year: 2010

We tested the hypothesis that vestibular and cardiac rhythms compete to modulate muscle sympathetic nerve activity (MSNA) in human subjects. Sinusoidal galvanic vestibular stimulation was applied across the mastoid processes at each subject's cardiac frequency and at ± 0.1, ± 0.2, ± 0.3 and ± 0.6. Hz. Cyclic modulation of MSNA was weakest at this central frequency (44.8 ± 2.3%; n = 8); significantly lower than when delivered 0.1. Hz lower (57.7 ± 3.3%) or 0.1. Hz higher (56.3 ± 3.3%) than this frequency. We conclude that vestibular inputs compete with baroreceptor inputs operating at the cardiac rhythm, with vestibular modulation of MSNA being lowest when competition with the baroreceptors is highest. © 2010 Elsevier B.V.

Foley P.,Prince of Wales Medical Research Institute
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids | Year: 2010

Three neuropathological features attracted the attention of Alzheimer in his examination of the brain of Auguste Deter: abnormal fibrillary structures, cortical depositions now termed "plaques," and glial proliferation, whereby he noted remarkable lipid granule accumulation in the glia. These features were also recorded by Perusini and Kraepelin, but by 1930 the lipoid deposits were no longer regarded by neuropathologists with great interest. © 2010 Elsevier B.V. All rights reserved.

Adlam A.R.,MRC Cognition and Brain science Unit | Patterson K.,MRC Cognition and Brain science Unit | Bozeat S.,MRC Cognition and Brain science Unit | Hodges J.R.,Prince of Wales Medical Research Institute
Neurocase | Year: 2010

The aims of this study were (a) to explore the utility of, and make more widely available, an updated and extended version of the Cambridge Semantic Memory test battery, and (b) to use this battery in conjunction with other tests to characterise the profile of several different forms of progressive cognitive impairment: semantic dementia (SD, n = 15), mild cognitive impairment (MCI, n = 7), established Alzheimer's disease (AD) (n = 8), all in comparison to normal controls (n = 45). The semantic battery is useful in a variety of ways for exploring the nature of semantic deficits; on its own, however, it does not provide sensitive differentiation between patients with AD and SD. An assessment including measures of episodic memory and visuospatial abilities as well as the semantic battery is recommended for good characterisation of the cognitive profiles associated with SD and AD. © 2010 Psychology Press.

Birznieks I.,Prince of Wales Medical Research Institute | Wheat H.E.,University of Melbourne | Redmond S.J.,University of New South Wales | Salo L.M.,University of Melbourne | And 2 more authors.
Journal of Physiology | Year: 2010

Torsional loads are ubiquitous during everyday dextrous manipulations. We examined how information about torque is provided to the sensorimotor control system by populations of tactile afferents. Torsional loads of different magnitudes were applied in clockwise and anticlockwise directions to a standard central site on the fingertip. Three different background levels of contact (grip) force were used. The median nerve was exposed in anaesthetized monkeys and single unit responses recorded from 66 slowly adapting type-I (SA-I) and 31 fast adapting type-I (FA-I) afferents innervating the distal segments of the fingertips. Most afferents were excited by torque but some were suppressed. Responses of the majority of both afferent types were scaled by torque magnitude applied in one or other direction, with the majority of FA-I afferent responses and about half of SA-I afferent responses scaled in both directions. Torque direction affected responses in both afferent types, but more so for the SA-I afferents. Latencies of the first spike in FA-I afferent responses depended on the parameters of the torque. We used a Parzen window classifier to assess the capacity of the SA-I and FA-I afferent populations to discriminate, concurrently and in real-time, the three stimulus parameters, namely background normal force, torque magnitude and direction. Despite the potentially confounding interactions between stimulus parameters, both the SA-I and the FA-I populations could extract torque magnitude accurately. The FA-I afferents signalled torque magnitude earlier than did the SA-I afferents, but torque direction was extracted more rapidly and more accurately by the SA-I afferent population. © 2010 The Authors. Journal compilation © 2010 The Physiological Society.

Pengas G.,University of Cambridge | Hodges J.R.,Prince of Wales Medical Research Institute | Watson P.,MRC Cognition and Brain science Unit | Nestor P.J.,University of Cambridge
Neurobiology of Aging | Year: 2010

Severe posterior cingulate cortex hypometabolism is a feature of incipient, sporadic Alzheimer's disease (AD). The aim was to test the hypothesis that this region is focally atrophic in very early disease by studying AD patients at the mild cognitive impairment (MCI) stage, and, if so, to determine whether the amount of atrophy was comparable to that of the hippocampus. Twenty-four patients meeting criteria for amnestic MCI, who all subsequently progressed to fulfil AD criteria, and 28 age-matched controls, were imaged with volumetric MRI. Four regions of interest were manually traced in each hemisphere: two posterior cingulate regions (BA 23 and BA 29/30), the hippocampus (as a positive control) and the anterior cingulate (as a negative control). BA 23 and BA 29/30 were both significantly atrophic and this atrophy was comparable to that found in the hippocampus, in the absence of anterior cingulate cortex (ACC) atrophy. Contrary to previous reports, there was no evidence that posterior cingulate atrophy is specifically associated with early-onset AD. The results indicate that posterior cingulate cortex atrophy is present from the earliest clinical stage of sporadic AD and that this region is as vulnerable to neurodegeneration as the hippocampus. © 2008 Elsevier Inc. All rights reserved.

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