We describe a unique case in which a patient was initially diagnosed with meningoencephalitis and then detected anti-myelin oligodendrocyte glycoprotein (MOG) antibody and demyelinating brain lesions. A 43-year-old Chinese man who complained of headache and fever, was diagnosed with meningoencephalitis after cerebrospinal fluid (CSF) analysis. One month after onset, brain imaging revealed multiple lesions in bilateral white matter, and the anti-MOG antibody was detected in his serum and CSF (titer is 1:32 and 1:10, respectively). After a 3-month glucocorticoid therapy, repeated brain imaging and serological analysis for anti-MOG antibodies showed significant improvement. Multiple intracranial demyelinating lesions secondary to meningoencephalitis may be accompanied by anti-MOG antibody positivity, which can be reversed by hormone therapy.

Astrocytes are promising source cells to replace neurons lost to disease owing to a shared lineage and capacities for dedifferentiation and proliferation under pathological conditions. Reprogramming of astrocytes to neurons has been achieved by transcription factor modulation, but reprogramming in vitro or in vivo using small-molecule drugs may have several advantages for clinical application. For instance, small molecules can be extensively characterized for efficacy, toxicity, and tumorigenicity in vitro; induce rapid initiation and subsequent reversal of transdifferentiation upon withdrawal, and obviate the need for exogenous gene transfection. Here we report a new astrocyte-neuron reprogramming strategy using a combination of small molecules (0.5 mM valproic acid, 1 μM RepSox, 3 μM CHIR99021, 2 μM I-BET151, 10 μM ISX-9, and 10 μM forskolin). Treatment with this drug combination gradually reduced expression levels of astroglial marker proteins (glial fibrillary acidic protein and S100), transiently enhanced expression of the neuronal progenitor marker doublecortin, and subsequently elevated expression of the mature neuronal marker NeuN in primary astrocyte cultures. These changes were accompanied by transition to a neuron-like morphological phenotype and expression of multiple neuronal transcription factors. Further, this drug combination induced astrocyte-to-neuron transdifferentiation in a culture model of intracerebral hemorrhage (ICH) and upregulated many transdifferentiation-associated signaling molecules in ICH model rats. In culture, the drug combination also reduced ICH model-associated oxidative stress, apoptosis, and pro-inflammatory cytokine production. Neurons derived from small-molecule reprogramming of astrocytes in adult Sprague-Dawley rats demonstrated long-term survival and maintenance of neuronal phenotype. This small-molecule-induced astrocyte-to-neuron transdifferentiation method may be a promising strategy for neuronal replacement therapy.

To date, only a few cases of intracranial infection related to severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) were reported. Here we describe a case of coronavirus disease 2019 (COVID-19) that was comorbid with purulent meningitis. A 62-year-old male patient was diagnosed with moderate COVID-19 and had no fever or cough after treatment. However, he suffered from a head injury and experienced headache and fever immediately after the accident. Computed tomography (CT) of the brain showed bilateral frontal lobe contusion, subdural hematoma, and subarachnoid hemorrhage. In the following days, the patient suffered from recurrent fever, although chest CT did not show evidence of worsening of infection. Several lumbar punctures were made, confirming increased cerebrospinal fluid (CSF) pressure and karyocyte count. SARS-CoV-2 nucleic acid was not detected in CSF but revealed the presence of Escherichia coli. Thus, the patient was diagnosed with purulent meningitis, presumably caused by brain trauma or the immunologic dysfunction caused by COVID-19, which was supported by the significant reduction of all kinds of immune cells. Since immunologic dysfunction is commonly presented in COVID-19 patients, comorbidity with meningitis should be considered when a COVID-19 patient presents with headache and fever. Lumbar punctures and CSF cultures may help in the diagnosis.

Mesenchymal stromal/stem cells (MSCs) are multipotent cells under consideration as a potential new therapy for a variety of inflammatory diseases including certain neurological disorders. It is generally thought that the efficacy of cell therapy in attenuating damage after ischemia, inflammation, or injury depends on the quantity of transplanted cells recruited to the target tissue. However, only a small number of systematically infused MSCs can effectively migrate to target sites, which significantly decreases the efficacy of exogenous cell-based therapy. In this review, we discuss specific factors influencing MSC migration, and summarize current strategies that effectively promote the motility of MSCs. In addition, we describe several protocols to improve the migration of stromal cells into the nervous system and, therefore, enhance the efficiency of engraftment as means of treating neurological disorders.

Stroke is a clinical disease with high incidence, high disability rate, and high mortality. But effective and safe therapy for stroke remains limited. Adult mesenchymal stromal cells (MSCs) perform a variety of therapeutic functions. MSC delivery improves neurological outcomes in ischemic stroke models via neurorestorative and neuroprotective effects such as angiogenic effects, promoting endogenous proliferation, and reducing apoptosis and inflammation. MSC secretome also showed powerful therapeutic effects as a cell-based therapy in animal experiments. Several clinical trials on MSC implantation via different routes have now been completed in patients with stroke. Although challenges such as immunogenicity of allo-MSCs and large-scale production strategies need to be overcome, MSCs can be considered as a promising potential therapy for ischemic stroke.