Background: Post-acute sequelae of COVID-19 (PASC) comprise a broad spectrum of symptoms such as fatigue, general weakness, compromised attention and sleep or anxiety disorders. PASC represents a medical and socio-economic challenge. Objectives: Our study evaluated cytokines (IL-1β, IL-6 and TNFα) and cortisol levels in a cohort of typical patients with PASC, suffering concentration problems, fatigue and difficulties finding words. Design: This was a prospective cohort study. Four groups were analysed and compared: those who had never contracted SARS-CoV-2 ( n = 13), infected but had no PASC ( n = 34), infected with former PASC that resolved ( n = 40) and patients with ongoing PASC after infection ( n = 91). Methods: Cytokine and cortisol serum levels were determined in patients’ blood samples. Results: Cytokine levels of IL-1β, IL-6, TNFα and cortisol levels did not differ between groups analysed. Conclusion: This may indicate a non-organic/psychosomatic genesis of PASC; further studies are needed to elucidate the underlying causes of PACS, and non-organic causes should not be overlooked.

Spinal muscular atrophy (SMA) is a motor neuron disorder leading to progressive loss of ventral horn neurons resulting in muscle wasting. Here we investigate the contribution of spinal astrocytes to the pathogenesis of late-onset SMA forms using a mouse model. Furthermore, we generated SMA-like astrocytes using survival of motor neuron (SMN) siRNA transfection techniques. In the SMA mouse model, the activation of spinal astrocytes and the reduction of the inward rectifier potassium channel K_ir4.1 and excitatory amino acid transporter 1 (EAAT1) were observed at postnatal day (P) 28, preceding the loss of spinal motor neurons appearing earliest at P42. Using SMA-like astrocytes, we could mimic the modulation of spinal astrocytes of the mouse model in a dish and perform electrophysiological assessments and functional assays. In SMA-like astrocytes, glutamate uptake was diminished due to a reduction in EAAT1. Furthermore, patch-clamp measurements revealed reduced potassium uptake into astrocytes with membrane depolarization. Additionally, exposure of healthy spinal motor neurons to a conditioned medium of SMA-like astrocytes resulted in increased firing frequency. These data demonstrate spinal astrocytes’ crucial role in the late-onset SMA forms’ pathogenesis.

Introduction: Deep brain stimulation is an established method for the treatment of neurological and psychiatric disorders. To elicit the underlying mechanisms and explore new stimulation targets, rodent models are necessary. Cable bound external stimulation or portable devices limit movement of the animals and influence behavioral experiments. Therefore, implantable, individually programmed devices are required. Experimental procedure: The stimulator consists of an 8bit-microcontroller mounted on a square electrical board (10 × 10 mm). External control is enabled by a magnetic reed contact, as running control serves a white LED, running modes are displayed by flash codes. Stimulation parameters could be programmed in the range of pulse width: 60–500 μs, amplitude: up to 300 μA and frequency: 10–500 Hz. Power is supplied by two standard batteries. The device was implanted in 8–10 weeks old BALBc-mice. Functionality was examined by electrical stimulation of nucleus accumbens area with standard parameters for mice and determination of c-fos levels in vitro in brain slices. Results: The implanted microstimulators were well-tolerated by the mice, without impairment of free movement. Coating, external control, and monitoring of function with LED flash code proved to be fully adequate. Stimulation with standard stimulating parameters of nucleus accumbens elicited strong c-fos elevation on simulation site. Conclusion: We present a fully implantable stimulator for freely moving mice that meets the urgent need for further research on the effects of deep brain stimulation in rodent models. It offers the possibility to conduct behavioral experiments for up to 30 days of stimulation.

Neurological manifestations during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic are of interest, regarding acute treatment and the so-called post-COVID-19 syndrome. Parkinson’s disease (PD) is one of the most common neurodegenerative movement disorders worldwide. Hence, the influence of SARS-CoV-2 and the COVID-19 syndrome on PD patients has raised many questions and produced various publications with conflicting results. We reviewed the literature, with respect to symptoms, treatment, and whether the virus itself might cause PD during the SARS-CoV-2 pandemic in SARS-CoV-2-affected symptomatic PD patients (COVID-19 syndrome). In addition, we comment on the consequences in non-symptomatic and non-affected PD patients, as well as post-COVID syndrome and its potential linkage to PD, presenting our own data from our out-patient clinic.

Background: Hereditary transthyretin amyloidosis (ATTR amyloidosis) is a rare, genetically heterogenous, and clinically variable autosomal dominant disease that severely reduces life expectancy. As treatment options grow, a proper diagnostic approach is mandatory especially in non-endemic regions with diverse genetic backgrounds.Methods: We examined 102 neuropathy patients at a German neuromuscular centre. Common causes of polyneuropathy were ruled out by medical history and extensive laboratory testing to define a cohort of patients with progressive polyneuropathy classified as idiopathic. Molecular genetic testing of the entireTTRgene was performed, and the detected amyloidogenic and non-amyloidogenic variants were associated with the observed clinical phenotypes and results of prior diagnostic testing.Results: Two of 102 patients tested positive for amyloidogenic mutations (p.Ile127Val and p.Glu81Lys), while a variant of unknown significance, p.Glu26Ser, was found in 10 cases. In both positive cases, previous negative biopsy results were proved by gene sequencing to be false negative. In case of the p.Glu81Lys mutation we detected clinical presentation (combination of severe polyneuropathy and cardiomyopathy), ethnic background (patient of polish origin, mutation only reported in Japanese families before), and disease course clearly differed from well-known cases of the same mutation in the literature.Conclusions: In conclusion, transthyretin hereditary amyloid polyneuropathy (ATTR-PN) should be considered in cases of otherwise idiopathic polyneuropathy. Sequencing of the four exons of theTTRgene should be considered the key step in diagnosis, while tissue biopsy possibly leads to false negative results.