J Neuropathol Exp Neurol Vol. 77, No. 3, March 2018, p. 177 doi: 10.1093/jnen/nly005 distinguish Alzheimer disease (AD)/aging-related tau pa- The Ins and Outs of CNS Dendritic thology from that of other tauopathies, including cortico- Cells (DC) basal degenerations, progressive supranuclear palsy and Pick disease. These mAbs have the potential to be very use- De Laere et al describe the roles and migratory pathways of DC ful reagents for dementia research and for clinical diagno- in human inflammatory CNS diseases, particularly multiple sis, particularly for distinguishing cases with mixed tau sclerosis, and corresponding animal models. They highlight pathologies. gaps in current understanding of these processes and summarize see page 216 how current MS therapies may affect DC migration patterns. see page 178 Selected Autophagy in Feline Niemann- Zika Virus in the Postnatal Brain Pick Disease Type C1 (NPC1) It is well established that immature (1st and 2nd trimester) LC3 accumulated in axonal balloonings of climbing fibers brains are susceptible to Zika virus infection resulting in mi- arising from subdivisions of the inferior olive in cats crocephaly and related pathologies. An ongoing question is suffering from NPC1 decreases following intrathecal whether the virus can persist and continue to induce brain in- 2-hydroxypropyl-beta cyclodextrin administration, thus sug- jury. Chimelli et al report on a child who lived 5 months post- gesting altered autophagy in certain cerebellar pathways and natally after a documented first trimester Zika infection. its amelioration with cyclodextrin. There was ongoing brain injury and evidence of persistent, see page 229 though difficult to identify, infection. see page 193 Tau Oligomers Appear Early in Vulnerable Subgroups of the Nucleus Basalis in the March Increased Microglial Colony Stimulating to Alzheimer Disease Factor 1 Receptor (CSF1R) Expression in the Tiernan et al used immunohistochemistry to study the dis- CNS of SIV-Infected Macaques tribution of tau oligomers within cholinergic basal forebrain CSF1R-mediated signaling is constitutive in microglia and (CBF) neurons in autopsy brains from 33 subjects across promotes cell survival, proliferation, and differentiation. the clinical continuum including normal cognition, mild Knight et al examine CSF1R signaling in the SIV/macaque cognitive impairment, and mild AD. They found that tau model of HIV infection. Their results show coordinate upre- oligomers were present in CBF neurons early in the disease gulation of both CSF1R and its ligand, CSF1, and implicate and that their accumulation mirrored the previously de- this signaling pathway in progressive HIV CNS disease. scribed caudal to rostral progression of cell loss within see page 199 CBF neuronal subgroups. They conclude that tau oligomer formation is an early event in the disease course that con- tributes to known patterns of selective vulnerability within Pediatric Chordomas: A New Perspective the CBF. A multicentric retrospective study of pediatric chordomas see page 246 examined clinical data along with treatment modalities and outcome. A histopathological/immunohistochemical grading b-Actin Cleavage Following Focal Ischemia system recently crafted for adults was also applied. The authors describe the results of these correlative studies. With the long-term goal of identifying neuroprotective mole- see page 207 cules that could be exploited therapeutically, Ye et al demon- strate a connection between actin cleavage and DNA fragmentation in the middle cerebral artery occlusion model Conformation-Dependent Anti-Tau Mono- in rats. A striking finding in this study is the inhibition of clonal Antibodies (mAbs) granzyme-mediated DNA fragmentation by intact actin Gibbons et al report the generation, characterization and in vitro. immunohistochemical application of 2 anti-tau mAbs that see page 260 V C 2018 American Association of Neuropathologists, Inc. All rights reserved. 177 Downloaded from https://academic.oup.com/jnen/article-abstract/77/3/177/4858387 by Ed 'DeepDyve' Gillespie user on 16 March 2018
Journal of Neuropathology & Experimental Neurology – Oxford University Press
Published: Mar 1, 2018
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