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posterior NS gain improvements, compared to lateral and anterior NS gains, yielding a common canal plane gain asymmetry of 20% at 5 weeks, suggest similar neural compensation mechanisms were active along VOR pathways. Unexpectantly, canal plane improvement was not replicated in pitch plane asymmetries.Aim To adapt, translate, and utilize the Dimensional Apathy Scale (DAS) in Amyotrophic Lateral Sclerosis (ALS) to the Spanish population. Method We recruited 104 ALS patients (67 of their caregivers) and 49 controls. Participants completed the Spanish-translated DAS, Geriatric Depression Scale- Short form. Patients were also administered the ALS Functional Rating Scale-Revised (ALSFRS-R). Caregivers additionally completed the informant/caregiver-rated Spanish-translated DAS. The DAS was translated to Spanish using a back-translation method. Test-retest and internal consistency reliability were examined. Divergent validity was assessed by comparing the DAS with the depression scale (GDS-15). Principal Component Analysis (PCA) was applied to explore the substructure of the Spanish DAS. Results The internal consistency reliability of self-rated Spanish DAS was 0.72 and of the informant/caregiver-rated Spanish DAS was 0.84. Correlations between self-rated DAS subscales and GDS-15 were not statistically significant, with a good test-retest reliability. PCA analysis showed a similar substructure to the original DAS. ALS patients had significantly higher Initiation apathy than controls. Additionally, ALS patient informant/caregiver-rated DAS Emotional apathy was significantly higher than the self-rated, with no significant differences observed in the Executive and Initiation subscales. No association was found between DAS and functional impairment using the ALS Functional Rating Scale (ALSFRS-R). Conclusion The Spanish translation of the DAS is valid and reliable for use in assessing multidimensional apathy in the Spanish population. Availability of the Spanish DAS will allow for future research to explore different apathy subtypes and their impact in ALS and other conditions.This study aims to investigate functional brain reorganization brought about by the loss of physical movement and sensory feedback in lower limbs in chronic spinal cord injury (SCI). Eleven paraplegia patients with SCI and 13 healthy controls (HCs) were recruited. The experimental task used was a visuomotor imagery task requiring subjects to engage in visualization of repetitive tapping movements of the upper or lower limbs. Blood oxygen level-dependent (BOLD) responses were captured during the experimental task, along with the accuracy rate and the response time. The SCI patients performed worse in the Rey Auditory Verbal Learning Test (RAVLT) and the Trail Making Test. SCI patients had a larger BOLD signal in the left lingual gyrus and right external globus pallidus (GPe) when imagining lower-limb movements. For the upper-limb task, SCI patients showed stronger BOLD responses than the HCs in extensive areas over the brain, including the bilateral precentral gyrus (preCG), bilateral inferior parietal gyrus, right GPe, right thalamus, left postcentral gyrus, and right superior temporal gyrus. In contrast, the HCs displayed stronger BOLD responses in the medial frontal gyrus and anterior cingulate gyrus for both upper- and lower-limb tasks than the SCI patients. In the SCI group, for the upper-limb condition, the amplitudes of BOLD responses in the left preCG were negatively correlated with the time since injury (r = -0.72, p = 0.012). For the lower-limb condition, the amplitudes of BOLD responses in the left lingual gyrus were negatively correlated with the scores on the Short Delay task of the RAVLT (r = -0.73, p = 0.011). Our study provided imaging evidence for abnormal changes in brain function and worsened cognitive test performance in SCI patients. These findings suggested possible compensatory strategies adopted by the SCI patients for the loss of sensorimotor function from the lower limbs when performing a limb imagery task.Hexanucleotide repeat expansion (HRE) in the chromosome 9 open-reading frame 72 (C9orf72) gene is the most common genetic cause underpinning frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). It leads to the accumulation of toxic RNA foci and various dipeptide repeat (DPR) proteins into cells. These C9orf72 HRE-specific hallmarks are abundant in neurons. So far, the role of microglia, the immune cells of the brain, in C9orf72 HRE-associated FTLD/ALS is unclear. In this study, we overexpressed C9orf72 HRE of a pathological length in the BV-2 microglial cell line and used biochemical methods and fluorescence imaging to investigate its effects on their phenotype, viability, and functionality. We found that BV-2 cells expressing the C9orf72 HRE presented strong expression of specific DPR proteins but no sense RNA foci. Transiently increased levels of cytoplasmic TAR DNA-binding protein 43 (TDP-43), slightly altered levels of p62 and lysosome-associated membrane protein (LAMP) 2A, and reduced levels of polyubiquitinylated proteins, but no signs of cell death were detected in HRE overexpressing cells. Overexpression of the C9orf72 HRE did not affect BV-2 cell phagocytic activity or response to an inflammatory stimulus, nor did it shift their RNA profile toward disease-associated microglia. These findings suggest that DPR proteins do not affect microglial cell viability or functionality in BV-2 cells. However, additional studies in other models are required to further elucidate the role of C9orf72 HRE in microglia.Background Microglia are key mediators of inflammation during perinatal brain injury. Selleck WRW4 As shown experimentally after inflammation-sensitized hypoxic ischemic (HI) brain injury, microglia are activated into a pro-inflammatory status 24 h after HI involving the NLRP3 inflammasome pathway. The chemokine (C-X-C motif) ligand 1 (CXCL1), and its cognate receptor, CXCR2, have been shown to be involved in NLRP3 activation, although their specific role during perinatal brain injury remains unclear. In this study we investigated the involvement of CXCL1/CXCR2 in brain tissue and microglia and brain tissue after inflammation-sensitized HI brain injury of newborn rats. Methods Seven-day old Wistar rat pups were either injected with vehicle (NaCl 0.9%) or E. coli lipopolysaccharide (LPS), followed by left carotid ligation combined with global hypoxia (8% O2 for 50 min). Pups were randomized into four different treatment groups (1) Sham group (n = 21), (2) LPS only group (n = 20), (3) Veh/HI group (n = 39), and (4) LPS/HI group (n = 42).
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