It arose in the left anterior cingulate cortex with a pseudo-polycystic appearance on neuroimaging. Histological features contained the “specific glioneuronal element” mimicking DNT Selleckchem Roxadustat and the components of distinct neurocytic rosettes with a center of neuropil islands and pilocytic astrocytoma resembling RGNT. Although the mechanisms of mixed glioneuronal tumor are far from being well-known, their co-existence might suggest a possible etiologic relationship between DNT and RGNT. “
“C. Soler-Martín, Ú. Vilardosa, S. Saldaña-Ruíz, N. Garcia and J. Llorens (2012) Neuropathology and Applied Neurobiology38, 61–71 Loss of neurofilaments in the neuromuscular junction

in a rat model of proximal axonopathy Aims: Rodents exposed to 3,3′-iminodipropionitrile (IDPN) develop an axonopathy similar to that observed in amyotrophic lateral sclerosis motor neurones, in which neurofilaments accumulate in swollen proximal axon segments. This study addressed the hypotheses that this proximal axonopathy is associated with loss of neurofilament proteins in the neuromuscular GS-1101 ic50 junctions and a progressive loss of neurofilaments

advancing in a distal-proximal direction from the distal motor nerve. Methods: Adult male Long-Evans rats were exposed to 0 or 15 mM of IDPN in drinking water for 1, 3 or 5 weeks, and their distal axons and neuromuscular junction organization studied by immunohistochemistry. Quantitative data were obtained by confocal microscopy on whole mounts of the Levator auris longus. Results: Benzatropine Muscles showed no change in the distribution of acetylcholine receptor

labelling in the neuromuscular junctions after IDPN. In contrast, the amount of neurofilament labelling in the junctions was significantly reduced by IDPN, assessed with two different anti-neurofilament antibodies. In preterminal axons and in more proximal axon levels, no statistically significant reductions in neurofilament content were observed. Conclusions: The proximal neurofilamentous axonopathy induced by IDPN is associated with an abnormally low content of neurofilaments in the motor terminals, with a potential impact in the function or stability of the neuromuscular junction. In contrast, neurofilaments are significantly maintained in the distal axon. “
“We report clinicopathological features of a 23-year-old woman with Down syndrome (DS) presenting with subacute myelopathy treated with chemotherapy, including intravenous and intrathecal administration of methotrexate (MTX), and with allogenic bone-marrow transplantation for B lymphoblastic leukemia. Autopsy revealed severe demyelinating vacuolar myelopathy in the posterior and lateral columns of the spinal cord, associated with macrophage infiltration, marked axonal loss and some swollen axons.