Neuroscience Collection 2023
Last updated
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 age-related hearing loss in bats, the identification of parenchymal border macrophages as cellular regulators of tau-mediated neurodegeneration, and botulinum neurotoxin constructs for the treatment of chronic pain. Download the special collection PDF here.
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Image © 2023 Konings et al.
Parenchymal border macrophages’ (PBMs) function impedes tau pathology and tau-mediated neurodegeneration, whereas tau pathology promotes PBM dysfunction associated with impaired CSF flow.
Bats exhibited age-related hearing loss. Bats are exposed to immense conspecific noise, but the frequency-dependent hearing loss was not correlated to the noise.
A new technique to make therapeutic botulinum neurotoxins via isopeptide bonding is described. The novel elongated botulinum neurotoxin can treat nerve injury pain without causing muscle paralysis.
Parkin, an E3 ubiquitin ligase involved in Parkinson’s disease, is inactive in the basal state and is activated by PINK1 to mediate mitophagy. Here, we characterized 31 mutations and discovered three that activate Parkin and rescue loss of PINK1 phosphorylation.
Apolipoprotein E4, the most important genetic risk factor for Alzheimer's disease, is shown to internalize into neurons and intersect with amyloid-β in endosomes–autophagosomes of neurites and modulate intraneuronal amyloid-β-42.
NDR1/2 kinases are essential for efficient endocytosis and protein clearance by autophagy. Neuron-specific dual deletion of NDR1 and NDR2 causes cortical and hippocampal neurodegeneration, implicating these kinases in neuronal protein homeostasis and health.
The protein sorting receptor SorCS1 shields the synapse organizer β-neurexins from amyloid-β oligomers (AβOs) to alleviate AβO-induced synaptic pathology.
This study adds insights into FTSJ1 tRNA 2′-O-methylation–associated pathologies in humans and Drosophila by identification of novel FTSJ1 targets and neuron morphology defects.
A lack of brain-synthesized IGF-I almost completely abrogates hippocampal long-term potentiation (LTP), alters spatial memory and sex-dependent behavior, and produces major changes in the mouse hippocampal proteome.
The authors suggested that an important role of Down syndrome critical region 1 (DSCR1) in microglial activation is to provide a potential therapeutic target for microglial Aβ clearance in Alzheimer’s disease.
