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Journal of Neuropathology & Experimental Neurology:
doi: 10.1097/NEN.0b013e31824d4998
In This Issue

In This Issue

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Distinguishing Microglia From Blood-Derived Monocytes in Inflammation Associated With Experimental Spinal Cord Injury (SCI)

Mawhinney et al used lysozyme M transgenic mice that express enhanced green fluorescent protein (EGFP) only in mature hematopoietic granulo-myelomonocytic cells and not in microglia to assess temporal and spatial relationships between microglia-derived and hematogenous macrophages in a SCI model. The 2 distinct macrophage populations could be independently identified and tracked, thereby allowing their roles in acute and chronic stages of SCI-associated inflammation to be defined.

see page 180

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Unmyelinated Axons Show Selective Rostrocaudal Pathology in the Corpus Callosum Following Traumatic Brain Injury (TBI)

Reeves et al identified preferential vulnerability of unmyelinated axons to degeneration following moderate fluid percussion TBI in adult rats. The finding has implications for current concepts of the functional significance of the responses of distinct axon populations following TBI and for development of specifically targeted therapies.

see page 198

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A Galvanizing Insight in Alzheimer Disease Model Mice

Lee et al identified age-dependent reductions in zinc transporter 3 (ZnT3) expression and altered synaptic Zn2+ levels in hippocampi of human βAPP-transgenic (Tg2576) mice. Zn2+ and ZnT3 expression were colocalized surrounding amyloid plaques, in dystrophic neurites and in reactive astrocytes. The results suggest a role of ZnT3 distinct from its roles in synapses and that an altered Zn2+ pool may underlie neuronal dysfunction in Alzheimer disease.

see page 211

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Hungarian Prions

In this comparison of prion proteins (PrP) in 6 cases of sporadic CJD with genetic CJD, 4 morphological types of PrP immunoreactivity were identified. One type displayed mutant PrP in autophagic vacuoles and aggresome-like structures, suggesting a cytoprotective mechanism.

see page 223

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Neuronal RNA Oxidation in Early Alzheimer Disease

Neuronal RNA oxidation is a prominent feature in age-associated neurodegenerative disorders such as Alzheimer disease (AD). Nunomura et al show that progressive neuronal RNA oxidation is an age-associated phenomenon and that more prominent RNA damage than in normal aging correlates with the onset of cognitive impairment in the prodromal stage of AD.

see page 233

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EphA4 in Human Traumatic Brain Injury

Ephs are membrane-bound tyrosine kinase receptors that, along with their ephrin ligands, are upregulated on reactive astrocytes in experimental TBI. Frugier et al studied EphA4 in brains from 19 patients who died following acute severe closed head injury and in cultured primary astrocytes. They found prolonged EphA4 upregulation near the injury and in the contralateral hemisphere. EphA4 activation induced by inflammatory mediators in vitro was inhibited using unclustered EphA4 ligand. These results suggest that blocking EphA4 activation may represent a therapeutic approach for TBI in humans.

see page 242

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At the Crossroads of Periventricular White Matter Injury Timing

Verney et al examined the astrocytic and microglial reaction at the crossroads of newly forming axonal tracks in the developing forebrain. Their data indicate these axonal crossroad areas are highly vulnerable in very preterm infants and highlight differences in the cellular response of very preterm vs. preterm infants.

see page 251

© 2012 American Association of Neuropathologists, Inc

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