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Targeting Neurotrophin and Nitric Oxide Signalling to Promote Recovery and Ameliorate Neurogenic Bladder Dysfunction following Spinal Cord Injury—Mechanistic Concepts and Clinical Implications
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Targeting Neurotrophin and Nitric Oxide Signalling to Promote Recovery and Ameliorate Neurogenic Bladder Dysfunction following Spinal Cord Injury—Mechanistic Concepts and Clinical Implications

  • Workshop 17
  • Thursday 8th September 2022
  • 07:30 - 09:00 CEST
  • Hall K1/2. Capacity: 400
  • In-Person and online attendees
  • ICS Members OnlyRestricted Video
25/12/2024 09:10:29

Workshop Schedule

07:30

Current Pharmacological Options for Treating SCI-induced LUT Dysfunction.

Karl-Erik Andersson

07:50

Treating SCI-induced LUT Dysfunction Using Neurotrophin/NO• Signaling Promotors.

Anthony John Kanai

08:15

Mechanism and Pathophysiology of SCI-induced NDO.

Christopher Henry Fry

08:40

Mechanism and Pathophysiology of SCI-induced DSD.

Naoki Yoshimura

Aims & Objectives

Advanced
90 minutes
Neurourology
Pure and Applied Science / Translational
Spinal Cord Contusion Detrusor-sphincter dyssynergia detrusor overactivity
Urology, Urogynaecology and Female & Functional Urology, Bowel Dysfunction, Pure and Applied Science

Spinal cord injury (SCI) causes impairment of mobility and neurogenic detrusor overactivity (NDO) that contribute to a decreased quality of life. This workshop will describe: i) the current state-of-the-art management of lower urinary tract (LUT) dysfunction associated with SCI; ii) the pathophysiology of this dysfunction; and iii) the therapeutic potential of three pharmacological agents to promote functional LUT recovery after SCI. These agents are: LM11A-31, a neurotrophin receptor modulator; LM22B-10, an agent that promotes neuronal growth; and cinaciguat, a soluble guanlyate cyclase activator that supports repair of spinal lesions. LM11A-31 and cinaciguat have passed human safety tests and may readily transition to clinical trials.