How do ALS-associated OPTN mutations mechanistically disrupt Rab8a binding and cellular function?

Analysis ID: SDA-2026-04-14-gap-pubmed-20260410-183548-043c7918 | Domain: neurodegeneration | Status: failed | Created: 2026-04-14T08:49:54.086044

Top Hypotheses (1 total)

#1 TREM2 Agonism to Redirect Microglia from Synaptic Pruning to OPTN-Deficient Neuron Protection

0.521

TREM2

# TREM2 Agonism to Redirect Microglia from Synaptic Pruning to OPTN-Deficient Neuron Protection ## Mechanistic Foundation: OPTN Deficiency and Microglial Recruitment Optineurin (OPTN) is a ubiquitin

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