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Thymomas have been associated with the generation of paraneoplastic autoantibodies to neurogenic epitopes, collapsin-response-mediator protein-5 receptor (CRMP-5) and alpha-amino-3-hydroxyl-5methyl-4isoxazolepropionic acid receptor (AMPAR), in patients with acute viral infection. We report a patient with thymoma and myasthenia gravis, with SARS-CoV-2 infection, who became comatose secondary to autoimmune encephalitis. Plasmapheresis, high-dose steroids, pyridostigmine, eculizumab, and rituximab did not restore neurologic function.

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  • Brown adipose tissue (BAT) is critical for energy consumption, and its dysfunction can lead to metabolic diseases and obesity, especially as we age.
  • The study identifies that perineurial cells, which have reduced antioxidant capacity due to lacking superoxide dismutase 2, impair BAT function by causing sympathetic nerve denervation and reducing fat oxidation.
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: Paraneoplastic neurological syndromes (PNSs) are rare conditions characterized by immune-mediated pathogenesis, frequently associated with the presence of a neoplasm. Although a single antineuronal antibody mediates a specific syndrome, atypical manifestations mediated by the same antibody have been described. : The aim of this study was to report on an atypical case of PNS with dual positivity for anti-GAD65 and anti-CRMP5/CV2 antibodies, simultaneously characterized by cognitive decline associated with progressive ataxia and parkinsonism.

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Paraneoplastic retinopathy (PR) is a rare autoimmune condition typically associated with progressive visual loss and is often linked to anti-recoverin antibodies. Paraneoplastic optic neuropathy (PON) is classically associated with collapsin response-mediator protein (CRMP-5). We present a unique case of non-progressive CRMP-5-associated perifoveal retinitis in a 79-year-old female with a history of breast carcinoma, who has maintained a stable visual acuity over an extended follow-up period of three years.

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Collapsin response mediator protein 2 (CRMP2) functions in the genesis and activity of neuronal connections in mammalian brain. We previously reported that a protein coincident with CRMP2 on 2D-gels undergoes marked accumulation of abnormal L-isoaspartyl sites in brain extracts of mice missing the repair enzyme, protein L-isoaspartyl methyltransferase (PIMT). To confirm and explore the significance of isoaspartyl damage in CRMP2, we expressed and purified recombinant mouse CRMP2 (rCRMP2).

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