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ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
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ALS - Motor Neuron Disease: Mechanism and Development of New Therapies

Published on: July 29, 2007

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ALS-related human cortical and motor neurons survival is differentially affected by Sema3A

Anastasya Birger1,2, Miri Ottolenghi2, Liat Perez1

  • 1Department of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada (IMRIC), Faculty of Medicine, The Hebrew University, P.O. Box 12272, 91120, Jerusalem, Israel.

Cell Death & Disease
|February 17, 2018
PubMed

Insights

Semaphorin 3A (Sema3A) differentially affects motor neuron survival. Upregulation in the cortex and downregulation in the spinal cord may contribute to motor neuron loss in amyotrophic lateral sclerosis (ALS).

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Amyotrophic lateral sclerosis (ALS) involves motor neuron (MN) cell death, with mechanisms not fully understood.
  • Semaphorin 3A (Sema3A) is implicated in neurodegeneration, showing altered levels in ALS patients.
  • Sema3A's role in MN survival is complex, with conflicting evidence from mouse models.

Purpose of the Study:

  • To investigate the direct effects of Semaphorin 3A (Sema3A) on human cortical neurons and spinal cord motor neurons (MNs).
  • To determine if Sema3A's differential expression in ALS contributes to MN cell loss.

Main Methods:

  • Culturing human cortical neurons and spinal cord motor neurons.
  • Exposing neurons to Semaphorin 3A (Sema3A) to assess survival rates.

Main Results:

  • Semaphorin 3A (Sema3A) enhanced the survival of human spinal cord motor neurons.
  • Semaphorin 3A (Sema3A) decreased the survival of human cortical neurons.
  • Observed differential effects align with Sema3A expression changes in ALS patients.

Conclusions:

  • Altered Semaphorin 3A (Sema3A) levels in the motor cortex and spinal cord may directly contribute to motor neuron degeneration in ALS.
  • Sema3A acts as a survival factor for spinal cord motor neurons but is detrimental to cortical neurons.
  • Understanding Sema3A's dual role is crucial for developing targeted ALS therapies.

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