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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.

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

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.

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.

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.

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.

An effective and reversible mouse glaucoma model that replicates the secondary glaucoma in human patients caused by silicone oil after retina surgeries presents significant neurodegeneration, and is suitable for neuroprotectants selection.

Axon degeneration occurs via an ordered sequence of events downstream of SARM1 that proceeds from ATP loss, to defects in mitochondrial movement and depolarization, followed by calcium influx, phosphatidylserine externalization, loss of membrane permeability, and ending with catastrophic axonal self-destruction.

Neurotrophin deprivation leads to rapid caspase-independent disassembly of the actin-spectrin-based membrane skeleton and spectrin-dependent retrograde signaling in axon degeneration.