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Natural selection is an evolutionary process in which individuals with survival-promoting traits reproduce at higher rates. These favorable traits become more common within a population or species. Naturally selected traits initially arise via random genetic mutations. In order for selection to occur, there must be variation within a population, the trait controlling the variation must be heritable, and there must be an evolutionary advantage for variation in the trait.
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ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
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[Motor neuron heterogeneity and selective vulnerability in ALS].

Hidemi Misawa1, Yuta Morisaki1

  • 1Division of Pharmacology, Faculty of Pharmacy, Keio University.

Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
|August 14, 2018
PubMed
Summary

Osteopontin (OPN) plays a dual role in amyotrophic lateral sclerosis (ALS) motor neuron degeneration. Targeting the OPN-integrin-MMP9 pathway may offer a novel therapeutic strategy for ALS.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Amyotrophic lateral sclerosis (ALS) exhibits selective vulnerability of motor neuron subtypes, with fast-fatigable (FF) neurons being most susceptible.
  • Osteopontin (OPN) and matrix metalloproteinase-9 (MMP9) are identified as markers for resistant (FR/S) and vulnerable (FF) motor neurons, respectively.

Purpose of the Study:

  • To investigate the role of osteopontin (OPN) in the differential vulnerability of motor neuron subtypes in a mouse model of ALS.
  • To explore the potential of the OPN-αvβ3 integrin-MMP9 axis as a therapeutic target for ALS.

Main Methods:

  • Utilized SOD1G93A transgenic mice as an ALS model.
  • Characterized OPN and MMP9 expression in motor neurons during disease progression.
  • Investigated the role of OPN through genetic ablation.

Main Results:

  • OPN accumulates extracellularly and is co-expressed with MMP9 in motor neurons around disease onset.
  • OPN-expressing motor neurons exhibit αvβ3 integrin and endoplasmic reticulum (ER) stress.
  • These OPN-positive neurons represent remodeled FR/S motor neurons compensating for initial FF neuron loss.
  • Genetic ablation of OPN initially delayed, but subsequently accelerated, ALS progression, indicating dual roles.

Conclusions:

  • OPN contributes to ALS pathogenesis through both cell-autonomous and non-cell-autonomous mechanisms.
  • OPN in FR/S motor neurons is implicated in a second wave of degeneration.
  • The OPN-αvβ3 integrin-MMP9 pathway presents a potential therapeutic target for ALS.