Neuroscience Collection 2022
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We are pleased to present this special collection of articles recently published in LSA highlighting some of the latest advances in neuroscience. Articles featured in the collection were published within the past 12 months and include original findings on optogenetic hearing restoration, the identification of a mutation underlying peripheral neuropathy, and pathogenic mechanisms that underlie neurodegenerative diseases such as Alzheimer’s disease. Download the special collection PDF here.
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Image © 2021 Woo et al.
Extracellularly delivered poly-GAs are internalised into astrocytes via an endocytosis-dependent pathway and then spread to motor neurons, implying non-cell autonomous mechanisms in C9ORF72-ALS/FTD.
This longitudinal study revealed stable expression of the fast-gating channelrhodopsin f-Chrimson in cochlear neurons of mice over at least 2 yr upon a single postnatal AAV dosing of the cochlea.
We present how reversible edema can reliably be induced in experimental cerebral malaria and show that it is associated with transcellular blood–brain barrier disruption and delayed microhemorrhages.
CIL-1 and ATLN-1 maintain the balance between ER tubules and sheets and prevent invasion of cortical ER sheets into the axon, contributing to the non-uniform distribution of neuronal ER-PM contacts.
Adult mouse choroid plexus shows elevated APP expression. sAPPα secreted into the CSF modulates neurogenic niche proliferation, whereas choroid plexus expression of fAD APP mutants leads to reduced niche proliferation, deficits in hippocampus synaptic plasticity, and learning defects.
This work studies known and new ADPRHL2 mutations with different disease mechanisms overall indicating that loss of nuclear ARH3 alone is pathogenic via dysregulated nuclear ADP ribosylation.
SMN deficiency leads to elevated ribosomal DNA damage that results in impaired ribosomal RNA synthesis and translation and is accompanied by a motor neuron-specific down-regulation of DDX21 protein.
GPCRs regulator, β-arrestin1, is increased in FTLD-tau patients, is required for β2-adrenergic receptor and metabotropic glutamate receptor 2-induced tau phosphorylation, promotes tau aggregation by impairing autophagy, and destabilizes microtubule dynamics, whereas genetic reduction in β-arrestin1 mitigates tauopathy and cognitive impairments.
The authors show in the mouse how the auditory hair cell structural maintenance is perturbed by the inactivation of Manf and the concomitant ER stress, causing early-onset, progressive hearing loss.