NDR Whitepaper Issue 1 (Thymopoietin)
Thymopoietin is a polypeptide hormone of the thymus. The pentapeptide thymopentin (TP-5) appears to represent the active site of thymopoietin, it has all the biological activities of the native hormone. The thymopoietin mimic levamisole HCl has some of the biological activities of thymopoietin. Both chemicals affect neuroinflammation and may be useful in neurodegenerative disease.
Proinflammatory cytokines, reactive oxygen species, and pro-inflammatory lipid-derived compounds result in neuronal damage and supply a positive feedback loop of neuroinflammation. Pathways of inflammation have multiple and redundant initiation sites and that means that many proinflammatory cytokines can compensate in the absence of any single factor.
NDR Whitepaper Issue 2 (Treatments are lacking)
NDR’s goals are simple, bring promising therapies to ALS patients and know which treatment is appropriate for a patient by evaluating biomarkers. Classically, the path to licensed treatment and testing drugs starts in the laboratory. Treatments are then tested in mice models of ALS, and then safety and effectiveness studies and conducted in people.
NDR Whitepaper Issue 3 (Secretome)
Adipose-derived stem cell conditioned media could be a treatment for ALS. The neuroprotective and regenerative effects of conditioned media were demonstrated in animal models for Parkinson’s disease hypoxic-ischemic brain injury, and peripheral nerve injury.
NDR Whitepaper Issue 4 (C9orf72)
The discovery of a repeat expansion1 in the C9orf72 gene is important because it is a model to explain central pathomechanisms of ALS.
NDR Whitepaper Issue 5 (Activity of thymosan)
Inflammation and regulation of inflammatory responses are necessary for life. Dysregulation of inflammatory pathways are fundamental elements of many neurodegenerative diseases. A pleotropic polypeptide hormone, thymopoietin was discovered by its effect on neuromuscular transmission.
NDR Whitepaper Issue 6 (Energy Metabolism)
Many chronic illnesses share common pathologic pathways so it may be anticipated that our paths lead in the same direction. Neurodegenerative disease pathologies disrupt the cell’s energy (mitochondria) which disturbs cell-to- cell communication causing inflammation, cell death, and metabolic disturbances.
NDR Whitepaper Issue 7 (Models of ALS)
Cathleen Lutz (Jackson Laboratory) described ALS as a “complex disease and consists of a group of conditions unified by a common theme, resulting in motor neuron degeneration and in many cases, convergent TDP-43 pathology. Importantly, the future for ALS therapeutics is no longer relegated to the concept of a single drug as a defining treatment, but rather opens the door for therapeutics that are stratified based on individual genes, pathways, or mechanisms.”
NDR Whitepaper Issue 8 (ALS and epigenetics)
Nothing illustrates that change is the essence of life quite like the butterfly. How does this cloudless sulphur caterpillar, eating the toxic blooms of a cassia bush, become a butterfly? How did it know the cassia toxin would protect it from predators ensuring a next generation? How did it select the bright colors that warn birds that it has a toxin and they should stay away? And how does it transform into the butterfly for the next phase of its life?
Stress Response in ALS