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IL6 Transsignaling and the IL6R Asp358Ala Polymorphism in Amyotrophic Lateral Sclerosis

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abstract
In distinct environments, both temporally and physically, interleukin-6 (IL6) has the potential to contribute to and be produced by pathology in amyotrophic lateral sclerosis (ALS). These roles are likely dependent on the local and systemic presence of the soluble IL6 receptor (sIL6R) and subsequent IL6 transsignaling. Production of IL6 by stressed muscle around the time of initial denervation or motor neuron dysfunction may initially maintain motor neuron (MN) axons and neuromuscular junctions (NMJs). However, in the central nervous system (CNS), transsignaling could fuel damaging neuroinflammation and gliosis, speeding up disease progression. In the lung, transsignling could propagate inflammation to otherwise healthy parenchyma and stimulate smooth muscle proliferation, thereby creating obstruction.
subject
Amyotrophic Lateral Sclerosis
Cytokine
Interleukin-6
Motor neuron
Neurology
Neuromuscular
contributor
Wosiski-Kuhn, Marlena (author)
Milligan, Carol E (committee chair)
Whitlow, Christopher T (committee member)
Caress, James B (committee member)
Cartwright, Michael S (committee member)
Hawkins, Gregory A (committee member)
Langefeld, Carl D (committee member)
date
2020-05-29T08:36:03Z (accessioned)
2020 (issued)
degree
Neuroscience (discipline)
2022-05-28 (liftdate)
embargo
2022-05-28 (terms)
identifier
http://hdl.handle.net/10339/96828 (uri)
language
en (iso)
publisher
Wake Forest University
title
IL6 Transsignaling and the IL6R Asp358Ala Polymorphism in Amyotrophic Lateral Sclerosis
type
Dissertation

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