<i>S</i>. <i>pinnatifida</i> extracts are neuroprotective against paraquat and oligomeric α-SN toxicity on dopaminergic neurons in primary mesencephalic cell cultures.

<p>(<b>A</b>) Box-Plot Graphic showing the effect of 1, 10, 100 and 1000 μg/ml to determine the non-toxic concentration of DCMEx (DCM) and BuOHEx / EtOAcEx (BE) on dopaminergic TH⁺ neurons. (<b>B</b>) Box Plot Graphic showing the toxic effect of paraquat, rotenone and an α-SN oligomer/monomer mixture on TH⁺ neurons and the protective effect of 100 μg/mL BuOHEx / EtOAcEx (BE) or 1 μg/mL DCMEx (DCM) against this aggression. (<b>C</b>) Box-Plot Graphic showing the effect of α-SN oligomers on ROS production in mesencephalic cells and its reduction in the presence of DCMEx, and BuOHEx / EtOAcEx. Whiskers represent Max and Min values. * represents <i>P</i> < 0.05, ** represents <i>P</i> < 0.01, n.s. non-significant.</p

Assessment the cytotoxicity of α-SN on PC12 cells in the presence of the extracts.

<p>(<b>A</b>) Cell viability measuring by MTT assay. PC12 cells were treated with 7 h-aged incubated α-SN in the absence and presence of different extracts. (<b>B-D</b>) Analysis of the cell death type using Annexin V/PI method: Living cell (Annexin V−/PI−) populations were located in the lower-left quadrant, the apoptotic cells were in the lower-right quadrant, late apoptotic (Annexin V+/PI+) populations were located in the upper-right quadrant, and necrotic cell (Annexin V−/PI+) populations were presented in the upper-left quadrant.(<b>E</b>) ROS production assay. Fluorescence intensity was measured at 480nm excitation and 520nm emission. The significance was set at <i>P</i><0.05.* The data are the means of three independent experiments ± SEM.</p

Table_1_Case report: Fatal Borna virus encephalitis manifesting with basal brain and brainstem symptoms.XLSX

BackgroundSince the first report of fatal Borna virus-1 (BoDV-1) encephalitis in 2018, cases gradually increased. There is a lack of diagnostic algorithm, and there is no effective treatment so far.Case presentationWe report an acute BoDV-1 encephalitis in a 77-year-old female with flu-like onset, rapid progression to word-finding difficulties, personality changes, global disorientation, diffuse cognitive slowness, and gait ataxia and further deterioration with fever, meningism, severe hyponatremia, epileptic seizures, cognitive decline, and focal cortical and cerebellar symptoms/signs. The extensive diagnostic workup (cerebrovascular fluid, serum, and MRI) for (meningo-)encephalitis was negative for known causes. Our empirical common antiviral, antimicrobial, and immunosuppressive treatment efforts failed. The patient fell into coma 5 days after admission, lost all brainstem reflexes on day 18, remained fully dependent on invasive mechanical ventilation thereafter and died on day 42. Brain and spinal cord autopsy confirmed an extensive, diffuse, and severe non-purulent, lymphocytic sclerosing panencephalomyelitis due to BoDV-1, affecting neocortical, subcortical, cerebellar, neurohypophysis, and spinal cord areas. Along with our case, we critically reviewed all reported BoDV-1 encephalitis cases.ConclusionThe diagnosis of acute BoDV-1 encephalitis is challenging and delayed, while it progresses to fatal. In this study, we list all tried and failed treatments so far for future reference and propose a diagnostic algorithm for prompt suspicion and diagnosis.</p