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Journal of Neuropathology & Experimental Neurology:
doi: 10.1097/NEN.0b013e3182a2d28f
In this Issue

In This Issue

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microRNAs (miRNAs) in Cerebral Ischemia-Induced Neurogenesis

Liu et al review current data on proliferation and differentiation of neural progenitor cells and migration of newly generated neuroblasts mediated by miRNAs in rodent stroke models. These studies lay the groundwork for amplifying neurogenesis to improve neurological outcome following cerebral ischemia and infarction in humans.

see page 718

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Getting Myoblasts to Stick

The transplantation of stem cells or myoblasts holds considerable promise for the treatment of many myopathies. One impediment to the integration of injected cells is having a receptive environment. Skuk et al show that electroporation of the muscle can enhance myoblast engraftment in a primate model.

see page 723

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Amyloid-β Inhibits Thrombospondin-1 (TSP-1) Release from Cultured Astrocytes: Effects on Synaptic Protein Expression

Thrombospondins are extracellular matrix proteins that in the CNS are predominantly produced by astrocytes and have been implicated in synaptogenesis. Rao et al suggest that amyloid-β mediates a reduction in astrocytic TSP-1 release that contributes to the loss of synaptophysin in neurons and thus leads to neuronal dysfunction in Alzheimer disease.

see page 735

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Calpain Activation and Preclinical Retinal Neurodegeneration in Autoimmune Optic Neuritis

Hoffmann et al demonstrate that calcium elevation and calpain activation in retinas and optic nerves and retinal ganglion cell degeneration precede a cellular inflammatory response in experimental optic neuritis in rats. This early neurodegenerative phase in this optic neuritis/MS model may be amenable to protective intervention using the calpain inhibitor calpeptin.

see page 745

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Improving Diagnostic Accuracy of Prion Diseases in Brain Biopsies with the Membrane Adsorption Assay (MAA)

Wemheuer et al compared the MAA with other techniques for diagnosing prion diseases in brain biopsies and autopsies. They found that the MAA is a useful tool for determining the presence of prion deposits as an initial diagnostic step that can increase the accuracy in confirming or excluding the presence of a prion disease.

see page 758

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Diffuse Traumatic Axonal Injury in the Optic Nerve Does Not Elicit Retinal Ganglion Cell (RCG) Loss

Using a mouse model of mild traumatic brain injury (TBI), Wang et al investigated RGC death. By several assays, they found no RGC loss from 2 to 28 days post-TBI, whereas traumatic axonal injury followed by disconnection was induced in the optic nerves. Their data highlight the distinction between diffuse axonal injury and traumatic nerve crush/transection injury mechanisms.

see page 768

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CD11c-Positive Cells in Retinas of CD11c-eYFP Transgenic Reporter Mice

CD11c-YFP mice are widely used for studies of resident microglia. Chen et al demonstrate the presence of congenital dystrophic lesions associated with activated microglia in the retinas of these mice. Recognition of these lesions is important for determining the cause of CD11c-positive putative dendritic cells vs. reactive microglia accumulations in neural tissues.

see page 782

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Dendritic Spine Density, Morphology, and Fibrillar Actin Content Surrounding Amyloid-β (Aβ) Plaques in a Mouse Model of Aβ Deposition

Kirkwood et al examined dendritic spines, including their f-actin content, in the cerebral cortex in a mouse model of Aβ deposition. Their findings suggest that strategies to preserve dendritic spines in patients with Alzheimer disease may need to address both non-fibrillar and fibrillar forms of Aβ and that non-fibrillar Aβ may exert spine toxicity through pathways not mediated by depolymerization of f-actin.

see page 791

© 2013 by American Association of Neuropathologists, Inc.