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Objective To undertake a randomized controlled trial in 196 obese subjects to examine the effect of electro-acupuncture on serum pro-oxidant antioxidant balance (PAB) values. Methods Subjects received authentic acupuncture (cases) or sham acupuncture (controls) for 6 weeks in combination with a low-calorie diet. In the following 6 weeks, they received the low-calorie diet alone. Serum PAB was measured at baseline, and 6 and 12 weeks later. Results We found that serum PAB values decreased significantly in the group receiving the authentic acupuncture compared to the sham treatment (p<0.001) at week 6, and whilst serum PAB increased significantly (p<0.05) in the second phase of the study, a significant difference between two groups remained at 12 weeks (p<0.05). Conclusions Electro-acupuncture in combination with a low-calorie diet was more effective at reducing serum PAB values in obese subjects compared to diet alone. Further work is required to determine the mechanism by which electro-acupuncture has this effect. [ABSTRACT FROM AUTHOR]

Background: The introduction of gene testing for Huntington's disease (HD) has enabled the neuropsychiatric and cognitive profiling of human gene carriers prior to the onset of overt motor and cognitive symptoms. Such studies reveal an early decline in working memory and executive function, altered EEG and a loss of striatal dopamine receptors. Working memory is processed in the prefrontal cortex and modulated by extrinsic dopaminergic inputs. Objective: We sought to study excitatory synaptic function and plasticity in the medial prefrontal cortex of mouse models of HD. Methods: We have used 2 mouse models of HD, carrying 89 and 116 CAG repeats (corresponding to a preclinical and symptomatic state, respectively) and performed electrophysiological field recording in coronal slices of the medial prefrontal cortex. Results: We report that short-term synaptic plasticity and long-term potentiation (LTP) are impaired and that the severity of impairment is correlated with the size of the CAG repeat. Remarkably, the deficits in LTP and short-term plasticity are reversed in the presence of a D1 dopamine receptor agonist (SKF38393). Conclusion: In a previous study, we demonstrated that a deficit in long-term depression (LTD) in the perirhinal cortex could also be reversed by a dopamine agonist. These and our current data indicate that inadequate dopaminergic modulation of cortical synaptic function is an early event in HD and may provide a route for the alleviation of cognitive dysfunction. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The neurobiology and neuropathology of the autism spectrum disorders (ASD) remain poorly defined. Brain imaging studies suggest that the deficits in social cognition, language, communication and stereotypical patterns of behaviour that are manifest in individuals with ASD, are related to functional disturbance and ‘disconnectivity’, affecting multiple brain regions. These impairments are considered to arise as a consequence of abnormal pre- and postnatal development of a distributed neural network. Examination of the brain post mortem continues to provide fundamental information concerning the cellular and subcellular alterations that take place in the brain of autistic individuals. Neuropathological observations that have emerged over the past decade also point towards early pre- and postnatal developmental abnormalities that involve multiple regions of the brain, including the cerebral cortex, cortical white matter, amygdala, brainstem and cerebellum. However, the neuropathology of autism is yet to be clearly defined, and there are several areas that remain open to further investigation. In this respect, more concerted efforts are required to examine the various aspects of cellular pathology affecting the brain in autism. This paper briefly highlights four key areas that warrant further evaluation. [ABSTRACT FROM AUTHOR]

Introduction: Cellular prion protein (PrPc ) is a normal glycosyl phosphatidylinositol-anchored protein expressed on a wide variety of cell types. Within the CNS, low levels of PrPc are particularly associated with neurons in normal healthy individuals. In contrast, a more pronounced expression of this protein may occur in certain neurodegenerative disorders (Esiri et al . Neuropath Appl Neurobiol 2000; 26: 273; Voigtlander et al . Acta Neuropathol 2001; 101: 417). Overexpression of PrPc has itself been reported to demonstrate neuropathology in transgenic mice (Westaway et al . Cell 1994; 76: 117). The present study investigated whether prion protein is up-regulated in two well-characterized neurodegenerative disorders: Alzheimer's disease (AD) and diffuse Lewy body disease (DLBD). Material and methods: Frozen material (frontal and occipital cortex) from cases with AD (n = 10), DLBD (n = 10) and neuropathologically normal brain (n = 10) were obtained from the MRC Brain Bank (Institute of Psychiatry, London), serially sectioned at 15–20 µm and immunoreacted in entire batches with four antisera to detect PrPc (3f4, sp40, 12f10 and F89/160.1.5) using the DAKO ABC method and DAB as chromogen. Sections from a case with Creutzfeldt-Jakob disease served as positive controls. Negative controls included preincubating test sections with proteinase K/guanidinium thiocyanate/formic acid, omitting primary antibody or incubation with nonspecific IgG. Immunoreactivity within selected brain regions was analysed using OPTIMAS image analysis software (OPTIMAS Corp., USA) on duplicate sections, and data processed as percentage immunoreactivity per defined field, based on a constant threshold (von Eitzen et al . JNEN 1998; 57: 246). The distribution of PrPc was further tested for correlation with glial reactivity (GFAP, PGM-1). Results: PrPc expression was mainly localized to the grey matter and was... [ABSTRACT FROM AUTHOR]

Introduction: One specific technique by which subdural haematoma can be timed has been one of the most challenging problems faced by pathologists. Currently, the most documented technique used for timing trauma is the Perl's stain for haemosiderin indicative of two days time lag between trauma and death. Trauma leads to the activation of a group of cells known as macrophages and offers a possible new means of timing trauma. The aim of this project was to reach a sensible conclusion about timing subdural haematoma by using a variety of markers against macrophages. Materials and methods: Using dural tissue from 28 subjects diagnosed with subdural haematoma, a three step amplification protocol (DAKO, UK) was applied to 5–7 µm sections of the dura, with DAB as chromogen, for subsequent light microscopic analysis. Results: Both qualitative (using a simple scoring system) and quantitative analysis were carried out in this study. Quantitative analysis comprised image capture using a digital camera mounted on a Zeiss axioplan microscope and image analysis by calculation of the percent areas of immunoreactivity per section using Optimas v6.2. Conclusions: PGM 1 and MHC II are not definitive at dating subdural haematoma within the first 48 h period. The early expression of these antibodies makes them good diagnostic tools for dating trauma when combined with other methods such as the Perl's stain. [ABSTRACT FROM AUTHOR]

Introduction: Microglia are resident mononuclear phagocytes of the central nervous system, which colonize the brain both prenatally and after birth. It is proposed that they enter the brain initially via the surrounding mesenchyme, via ventricles and later through blood vessels, but the mechanisms of entry and signals used for migration are still to be established. Previous studies have shown that ligands for some integrin adhesion molecules expressed on blood vessels in the developing nervous system (particularly ICAM-1 and ICAM-2 which bind CD11a/LFA-1 and CD11b/Mac-1), may act as potential recruiting signals for microglial precursors. This study addressed whether CD11b is influential on the migration of microglial precursors into the developing CNS. Material and methods: Ricinus communis agglutinin-1 (RCA-1) lectin histochemistry was employed to anatomically map the distribution of amoeboid and ramified microglia from embryonic day 15 (E15) to birth. Embryonic mouse brains from CD11b knockout (-/-) (n = 42), and heterozygote (+/-) (n = 52) mice generated on a C57/BL6 background (Melo et al . Cell Immunol 2000; 205: 13–23) and wild-type (+/+) (n = 37) litter mates were fixed in Bouin's solution, processed to paraffin wax and serially sectioned at 15–40 µm. To investigate further potential signals for recruiting microglial precursors, brains were immunochemically screened for integrins CD11a, CD11b, CD18, αX, VLA-4 and the chemokine MCP-1. Results: Microscopic analysis revealed the morphological transition of microglia from predominantly amoeboid forms at E15–E16 to a flourishing population of ramified cells at E19–E20. RCA-1 histochemistry showed no clear differences in microglial distribution or timing of colonization between CD11b (-/-) and wild-type mice from E15 to birth. Although CD11b deletion did not influence the timing of microglial ramification, there appeared to be fewer ramified cells in (-/-) mice within... [ABSTRACT FROM AUTHOR]