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Chemogenetic silencing reveals that entorhinal neurons require ongoing activity for survival, suggesting that their normal physiology may render them vulnerable to pathologies that impair transmission.

The identification of the mechanism of action of vacor, an environmental neurotoxin which causes neurodegeneration by activating the pro-degenerative enzyme SARM1, raises important questions on SARM1 as a mediator of environmental neurotoxicity and has implications for drug discovery.

GDNF receptor-expressing mesenchymal progenitor subpopulation within skeletal muscle responds to peripheral nerve injury by sensing GDNF and secreting BDNF, thereby directly promoting nerve regeneration through facilitating remyelination by Schwann cells.

While semantic symptoms in fronto-temporal dementia patients were mainly dependent on short-range white-matter fibre disruption, long-range white-matter fibres damage was the major contributor to executive dysfunction, highlighting the importance of controlling for risk factors associated with deep white-matter disease.

Local deep hypothermia combined with hibernation-mimicking cold protection is neuroprotective in a translatable large animal model of traumatic optic neuropathy.

Cryo-EM shows that the NADase activity of SARM1 is allosterically inhibited by physiological concentrations of NAD+ that stabilizes an auto-inhibited conformation of SARM1, explaining how NAD+ depletion may inflict neurodegeneration.

Upon traumatic brain injury in Drosophila adults, a previously unknown Pvr–AP-1–Mmp1 signaling pathway is activated in astrocytes.

ATP imaging of spiking optic nerve axons in real time reveals correlation between ATP levels and electrical activity as well as contribution of lactate metabolism to axonal ATP homeostasis.

Membralin mutant mice manifest a severe and early-onset motor neuron disease with defects in endoplasmic reticulum-associated protein degradation.