Canine degenerative myelopathy (DM) develops at a high incidence in homozygotes for the c118G>A SOD1 mutation and low incidence in heterozygotes. In vitro, wild-type and DM mutant SOD1 can interact, possibly as dimers and can form aggregates. Wild-type SOD1 can form dimers with various mutations of SOD1-associated fALS. However, unlike DM the majority of fALS with SOD1 mutations are heterozygous except the D90A mutation which is inherited in both recessive and dominant form.

The novel identified hyperekplexia mutant in the glycine transporter 2 GlyT2^P429L results in loss of function. Moreover, the mutant is associated with significantly decreased expression levels. The mutation leads at the structural level to a disruption of the integrity of the α-helix 5 and thus conformational changes localized in close proximity to the sodium binding site of the transporter.

In patients with glioma, a less segregated organization of the contralesional hemisphere (reflected by lower local efficiency) is associated with better reaction time scores. Better cognitive flexibility and better complex attention scores are associated with a better spread of information over the contralesional hemisphere through mutually interconnected hubs (reflected by higher assortativity). These results underline the importance of the contralesional hemisphere to cognitive performance.

The cold pressor test (CPT) reduces the magnitude of auditory evoked potentials (AEPs). This indicates that during CPT, supraspinal modulatory mechanisms (possibly attentional ones) are recruited.

We measured EEG in Gilles de la Tourette patients (GTS) and healthy controls. We tested whether tic inhibition influences the activity of the sensorimotor cortex during a motor task. GTS showed lower levels of beta modulation over the sensorimotor cortex during the execution of the task. This abnormal pattern returned to be normal during tic voluntary inhibition. We demonstrated that voluntary tic inhibition normalized the beta EEG rhythm of the sensorimotor cortex.

In fibromyalgia syndrome (FMS), altered gray matter volume (GMV) has been shown but with missing disease specificity. Regional voxel-based morphometry showed increased GMV in the precentral gyrus and decreased GMV in the angular and middle temporal gyrus in patients with FMS and another pain group in comparison with healthy controls. Since no GMV differences between both pain groups were obvious, cortical changes in FMS are not disease-specific but reflect alterations of chronic pain in general.

Ventral tegmental area glutamatergic (VGluT2) neurons differentially express calcium-binding proteins. A subpopulation of ventral tegmental area VGluT2 neurons expressing calbindin (VGluT2-calbindin) targets the nucleus accumbens (nAcc) shell.

Unilateral cochlear ablation causes mitosis confined to microglia within the affected cochlear nucleus. Many dividing microglia start expressing the purinoceptor P2X4. The absence of dying cells indicates a stable number of neurons and astrocytes through this period of tissue reorganization. While neurons neither die nor proliferate, they change processivity of DNA polymerases, indicating plastic responsiveness on the level of gene management.

Primate visual thalamus is traditionally segregated into a relay nucleus (dorsal lateral geniculate nucleus, LGN), and association nuclei including inferior pulvinar (IPul) and lateral pulvinar (LPul). We show in the marmoset brain that koniocellular layers of LGN and the central lateral (CL) division of IPul show common patterns of calbindin immunoreactivity and connectivity with the visual cortex, implying a functional congruity and anatomical continuity.

Using a rat model of infantile spasms with malformation of cortical development, we could prove the dose-dependent efficacy of methylprednisolone on spasms. Moreover, multiple doses of methylprednisolone lead to in vivo neurochemical changes with increased glutamate concentration in the cortex and electrophysiological changes in fast oscillations in the neocortex with reduced spasms susceptibility. These in vivo neurochemical and electrophysiological changes caused by methylprednisolone can be more therapeutic evidence of steroids in neurological disorders, including epilepsy.