@Cathy Pascale I thought this was answered. I'm just starting to get the hand of this platform. Let me post what I got.

Self-assembling hydrogels—such as the peptide-based injectable materials developed in ongoing MIT research—are designed to support peripheral nerve regeneration, not systemic neurodegenerative conditions like ALS. These gels form a 3D biomimetic scaffold after injection, guiding axons across an injury site, reducing local inflammation, and preventing scar formation. This is effective primarily in localized peripheral nerve injuries, such as cut or crushed nerves, where the upstream neuron cell bodies remain intact. ALS (amyotrophic lateral sclerosis) is a fundamentally different biological problem. Instead of localized injury, ALS involves widespread degeneration of motor neurons in the cortex, brainstem, and spinal cord. The disease is driven by toxic protein misfolding, including TDP-43, SOD1, and FUS, with evidence of prion-like spread of these misfolded proteins through neural pathways. Because the underlying pathology is diffuse and progressive, a localized hydrogel scaffold cannot address the core mechanisms that cause motor neurons to die throughout the nervous system. Although these hydrogels are not a treatment for ALS, they are beginning to appear in ALS-adjacent research in three main ways: 1. Stem-cell delivery support: Hydrogels are used as carriers for glial or stem cells delivered to the spinal cord. The material protects transplanted cells, improves survival, and distributes them more evenly across the cord. 2. 3D disease modeling: Hydrogel platforms are used to build neuromuscular junction and spinal-motor-unit models for drug screening, allowing researchers to study ALS pathology in more realistic environments. 3. Localized tissue support: In some animal studies, hydrogels deliver growth factors or therapeutic molecules to muscle or spinal tissue, providing local protective effects. Overall, self-assembling hydrogels represent an important biomaterial technology for regeneration, modeling, and drug delivery, but they are not currently capable of reversing or halting ALS, which requires interventions targeting protein misfolding, neuroinflammation, and widespread motor neuron loss.