Item Details

title

IL6 Transsignaling and the IL6R Asp358Ala Polymorphism in Amyotrophic Lateral Sclerosis

author

Wosiski-Kuhn, Marlena

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

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)

2022-05-28T08:30:13Z (available)

2020 (issued)

degree

Neuroscience (discipline)

embargo

2022-05-28 (terms)

identifier

http://hdl.handle.net/10339/96828 (uri)

language

en (iso)

publisher

Wake Forest University

type

Dissertation