OUP Neuro Hub: Neurocritical care collection
In the second collection of OUP’s Neuro Hub, we’ve organized more than 70 book chapters, journal articles, and entries from our reference products on neurocritical care.
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Orlandi et al. show that tau burden and MRI volume in progressive supranuclear palsy speech/language are greater in the frontal cortex but lower in subcortical/brainstem nuclei than Richardson’s syndrome. Clinical variability is, therefore, related to shifts in burden across a network of regions.
Gurholt et al. report that traits relevant to sarcopenia, a muscle disorder linked to body and brain impairments, are associated with lower general cognitive performance and brain structure phenotypes. Sensorimotor brain structures mediated the link between sarcopenic and cognitive traits. The findings provide essential cues for understanding the sarcopenia–dementia link.
De Albuquerque et al. report the potential of serum myostatin and follistatin levels as biomarkers for spinal muscular atrophy, encompassing research with animal models and humans. Myostatin levels were reduced in the disease, correlated with a disease severity and progressed over time, suggesting its utility as disease severity and progression biomarker.
Bondulich et al. show that levels of NEFL, total-Tau and BRP-39 in plasma and CSF will provide translatable readouts for preclinical studies in Huntington’s disease mouse models. Further analysis in mice may shed light on the underlying pathologies leading to elevated biomarker levels.
Leister et al. report that immunoproteasome deficiency results in spontaneous seizures and other brain pathologies such as tau hyperphosphorylation, degeneration of Purkinje cells and increased anxiety in aged mice. This suggests that the upregulation of immunoproteasomes during ageing affords protection from the exaggerated accumulation of protein aggregates and epilepsy development.
Hong et al. determined whether polyglutamine disease-associated CAG repeats modify Huntington's disease (Huntington’s disease). Analysis of typed and imputed tandem repeats did not support significant associations between the sizes of CAG repeat of other polyglutamine disease-causing genes and Huntington’s disease age-at-onset while revealing potential modification signals for tandem repeats at other loci.See J. Hannan (https://doi.org/10.1093/braincomms/fcae047) for a scientific commentary on this article.
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