In the recent pandemic disease, called COVID-19, the role of neurologists and neurobiologists represents a chance to study key features of brain infection and deepen neurological manifestations of COVID-19 and other coronavirus infections. In fact, many studies suggest brain damage during infection and persistent neurological symptoms after COVID-19 infection. Reverse transcription PCR test, antibody tests, Magnetic Resonance of lung, and Computed Tomography of brain of the patient were periodically performed during this case report for eight months after infection. The aim of this article is to describe the prolonged neurological clinical consequences related to COVID-19. We believe it is clinically clear that we can define a post-acute COVID-19 neurological syndrome. Therefore, in patients after a severe clinical condition of COVID-19, a deepening of persistent neurological signs is necessary.

Blood levels of total homocysteine (tHcy), cysteine (Cys), total and reduced glutathione (tGSH and rGSH), folic acid (FA), and vitamin B12 (B12) change during ischemic stroke as accompaniment of the tissue damage. The relationship between these changes remains scantly investigated. We evaluated the variation of these molecules in the 48 h after acute large artery atherothrombotic stroke (LAAS) and searched for the presence of matched variation of them. The study involved 50 subjects affected by acute LAAS and 49 healthy controls. Plasma levels of tHcy and Cys were significantly higher and serum levels of FA and B12 and plasma levels of rGSH were significantly lower in the patients than in the control group. Acute LAAS was associated with increased Hcy-decreased tGSH and decreased FA/tGSH. Pathways involved in cellular stress and in tissue repair are activated during acute LAAS.

Mounting evidence highlights the involvement of inflammatory/immune systems and their relationships with neurotransmitters and different metabolic processes in mood disorders. Nevertheless, there is a general agreement that available findings are still inconclusive. Therefore, further investigations are required, aimed at deepening the role of possible alterations of biomarkers in the pathophysiology of mood disorders that might lead to more focused and tailored treatments. The present study is a comprehensive review on these topics that seem to represent intriguing avenues for the development of real innovative therapeutic strategies of mood disorders.

Posterior reversible leukoencephalopathy (PRLE) is a neurological disorder caused by a variety of pathological conditions such as high doses or long-term low-doses of immunosuppressive therapy. PRLE associated with methotrexate (MTX) is well known but it was rarely observed in adult patients submitted to long-term low-dose administration via the oral route. Here we report the case of a patient affected by psoriasis, treated by chronic oral low-dose of MTX, who presented with limb ideomotor apraxia. Magnetic resonance (MRI) of the brain showed, on T2-weighted images, a diffuse hyperintensity involving bilaterally the white matter of the occipital, parietal and frontal lobes. MTX treatment was stopped and, at the 6-month follow-up, the neuropsychological performances was improved. Two years later, the neuropsychological profile was normal and MRI showed a regression of the white matter abnormalities.

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