neurite outgrowth

Keeping axons alive after injury: Inhibiting programmed axon death

Activation of pro-degenerative protein SARM1 in response to diverse physical and disease-relevant injuries triggers programmed axon death. Original studies indicated substantially decreased levels of SARM1 were required for neuroprotection. However, we demonstrate that lowering SARM1 levels by 50% in Sarm1 haploinsufficient mice delays axon degeneration in vivo (after sciatic nerve transection), in vitro (in response to diverse traumatic, neurotoxic, and genetic triggers), and partially prevents neurite outgrowth defects in mice lacking pro-survival factor NMNAT2. We also demonstrate the capacity for Sarm1 antisense oligonucleotides to decrease SARM1 levels by more than 50% which delays or prevents programmed axon degeneration in vitro. Combining Sarm1 haploinsufficiency with antisense oligonucleotides further decreases SARM1 levels and prolongs protection after neurotoxic injuries. These data demonstrate that axon protection occurs in a Sarm1 gene-dose responsive manner and that SARM1 lowering agents have therapeutic potential. Thus, antisense oligonucleotide targeting of Sarm1 is a promising therapeutic strategy against diverse triggers of axon degeneration.

Microfluidic high-throughput screening platform to screen pre-clinical stage compound effects on neurite outgrowth of human motor neurons post injury

BET protein inhibition in macrophages enhances dorsal root ganglion neurite outgrowth in female mice

Caffeine treatment decreases MAO-B expression, neurite outgrowth, and neurite branching in immature rat primary neuronal cell cultures

FENS Forum 2024

Human pluripotent stem cell-derived ectomesenchymal cells promote neurogenesis and neurite outgrowth in rats with hypoxic-ischemic brain injury through the ERK/CREB signaling pathway

FENS Forum 2024