There have been many attempts to repair nervous system damage, the most recent trend is to use electronic devices to bridge a signalling gap around an insult. These have all predictably failed despite early promise, in my opinion because they still carry a neuron-centric/electric brain view of nervous system function which has fairly significant flaws.
Over the past few months, a lot of work has been released exploring the mechanics of glia on a much more granular level, particularly astrocytes. In this work, there’s a clear pattern emerging that astrocyte local environments are unique and distinct in order to interpret and ultimately transmit the signals which travel within neurons (neurons are mostly agnostic to the signal, it’s the ends which connect into astrocyte local environments which give neurons unique signal properties). When these environments are disrupted, signalling fails to propagate and eventually degeneration of the cellular population around the insult occurs.
This is how life seems to be designed, first slowing the effect of the insult with inflammation then cementing the gap so signalling to the insulted area cannot continue in the area longer term. Other glial cells then attempt to repair as much of the local environment around the insult as possible (usually via microglial pruning). This process is similar to our vascular processes as well.
Every astrocyte local domain represents a distinct processing environment with unique information, which contributes to overall system processing. Think of each astrocyte as it’s own small co-processor responsible for managing that specific area of space. When these local groups are damaged, the nervous system loses information.
One of the really exciting trends I’m seeing is work which is geared toward allowing astrocytes to recreate new local domains within insulted areas, rather than assuming that only the “brain” generates or shapes signals. To this end there’s some recent work which is geared toward not just creating a “bridge” or “fill”, but allowing astrocytes to re-establish local domains through these areas and re-acquire/re-establish the necessary information to re-establish prior function.
Based on the rate of progress, we are likely to start seeing mega breakthroughs for spinal injury within the next few years. As in, we should be able to restore injury and stroke related processes with better than 80% efficacy. I acknowledge the optimism of this compared to prior results, however we are genuinely in completely new territory right now. We’ve been so limited by the neuron centric/brain centric view of function that this was literally impossible in the past.
Eventually (> 5 years at least) this type of work will spread to broader degenerative conditions with larger and more complex insults. And once we’ve mastered the metabolic control necessary to do that, it’s likely we’d be on the verge of either significantly or indefinitely extending lifespans.
I don’t want to be too hyperbolic and say that this feels like the alchemy->chemistry transition (because that was an extremely uneven process with lots of lessons in and of itself), but recent work has left me distinctly hopeful that we are on the precipice of significant improvements in functional outcomes for all information related biological processes.
Extra Reading – Glia as a key factor in cell volume regulation processes of the central nervous system
IL-12p40 promotes secondary damage and functional impairment after spinal cord contusional injury
Mechanistic stoichiometric relationship between the rates of neurotransmission and neuronal glucose oxidation: Reevaluation of and alternatives to the pseudo-malate-aspartate shuttle model – The assumptions here are wrong (and kind of garbage), but information transfer as an artifact of manipulation of stoichiometric balance is really important.
Transplantation of Human Induced Pluripotent Stem Cell-Derived Neural Progenitor Cells Promotes Forelimb Functional Recovery after Cervical Spinal Cord Injury – MDPI but decent researchers.
Connexins Signatures of the Neurovascular Unit and Their Physio-Pathological Functions