Santiago Loya‐López

This study identifies peripheral nociceptor hyperexcitability as a mechanism underlying pain in DM1 using a mouse model.

This study identifies NaV1.7-dependent peripheral sensitization as a mechanism of chronic pain in Parkinson's disease and highlights CRMP2 regulation of NaV1.7 as a therapeutic target.

This study shows that transient myotonia can cause long-lasting pain by altering nociceptive processing and identifies NaV1.8 as a target for analgesics.

This study shows that NRP1 in CGRP afferents is required for VEGFA-driven pain and baseline nociception in mice.

This paper introduces a method to preserve human dorsal root ganglion neurons using Hibernate media, enabling easier access and transport for research.

This study investigates how anti-CV2/CRMP5 autoantibodies cause pain in paraneoplastic neurological syndromes and identifies potential treatments.

The paper develops a CRMP2-Ubc9 inhibitor that reduces NaV1.7 activity and alleviates trigeminal neuropathic pain in rats.

The paper identifies a unique NaV1.7 domain that can be targeted to produce analgesia by disrupting its interaction with CRMP2.