Wallerian Degeneration Drug Discovery Service

Introduction of Wallerian Degeneration

Wallerian degeneration is an active process of retrograde degeneration that occurs when a nerve axon breaks and the nerve fibers distal to it degenerate. This phenomenon can be observed in many neurodegenerative diseases, such as Amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD). In general, Wallerian degeneration occurs within 24-36 hours of the peripheral nervous system (PNS) and central nervous system (CNS) axonal injury. Wallerian degeneration can always instigate the nerve repair mechanism, while cryotherapy, exercise, neurorehabilitation, and surgery are effective methods to manage nerve damage.

Pathological Process of Wallerian Degeneration

There are mainly 3 stages for the pathological process of Wallerian degeneration, including axon degeneration, myelin clearance, and regeneration.

• Axon degeneration: The proximal and distal ends of the nerve will rapidly separate within 30 minutes of injury
• Myelin clearance: Macrophages clear axons and myelin debris on day seven, while PNS shows higher efficiency of myelin debris removal than CNS.
• Regeneration: Injuries at the ends of axons regenerate at a rate of 1 mm per day.

Fig.1 The cytokine network of Wallerian degeneration. (Rotshenker, 2011)

Clinical Presentation of Wallerian Degeneration

• Neuromatous or burning pain
• Extremely sensitive to touch
• Muscle weakness or paralysis
• Lack of coordination
• Gradual numbness, tingling or tingling in the feet or hands
• Functional problems with damaged nerve-related structures

Mechanism and Treatment for Wallerian Degeneration

Innate immunity is central to Wallerian degeneration. The innate immune response helps to transform peripheral nerve tissue into an environment that supports regeneration. In this case, Wallerian degeneration would be served as a prelude for a successful repair. Recent studies have shown that sterile alpha and TIR motif-containing 1 (SARM1) protein plays an important role in the Wallerian degeneration pathway. What's more, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is essential for axon growth and survival, so the deficiency of the essential axonal protein NMNAT2 is a critical initiating event. Overexpression of NMNAT may rescue axons from degeneration. In many disease models, the Wallerian degeneration protein (WLDS) has the ability to delay axon loss and sometimes symptoms. Stem cell intervention now holds promise as a potential treatment option to enhance regeneration

What We Can Do About Wallerian Degeneration?

Creative Biolabs is a leading service provider that focuses on neuroscience research. We are confident in offering the best products and services for our clients all over the world. At Creative Biolabs, we have the expertise to optimize each stage of wallerian degeneration research to ensure that you get the results you want and achieve the highest level of efficiency. If you are interested in our services and products, please do not hesitate to contact us for more details.

Reference

1. Rotshenker, S. Wallerian degeneration: the innate-immune response to traumatic nerve injury. Journal of neuroinflammation. 2011, 8(1): 1-14.