The brain has redundancy at the level of neurons: it is quite resilient against diffuse neuron loss, and in case of localized damage, unless the affected area is large or includes key regions such as the brainstem, impairment is often limited to one or a few functions, and in some cases it even reorganizes to transfer the lost functions to other areas, partially recovering them.
However, there is no expectation that the brain has redundancy against the loss of an information storage medium that is used in all neurons.
If you destroy half of your collection of DVDs, the information in the other half is still intact. If you destroy every odd-numbered track on all of your DVDs, instead, most of the remaining data will be too fragmentary to be of any use, even if the number of bits you destroyed is the same in both cases.
There can be a lot of redundancy within neurons as well. Just because you find causally relevant chemical densities that predict neuron states doesn’t mean that there aren’t other chemical densities that also predict those same states.
Is there any evidece of such large redundancy at the level of biochemical information storage? I’m not aware of it, and I can’t see a good reason for such thing to have been evolved.
I’m not a neuroscientist, but AFAIK, I’m not sure that talking about chemical densities is the most appropriate way to frame the discourse here: synapses are small enough that the discrete nature of protein complexes and structures becomes relevant. While disrupting a single molecule wouldn’t significantly affect the neuron state, a process that causes generalized misallignment between the active zones on one side and corresponding receptors on the other side, or between the two halves of electric gap junctions, or other widespread distortions, could easily do. Unless this process is reversible in the information-theoretic sense, these bits of information are lost forever.
IIUC, the type of distortions that occur during cryopreservation: membrane deformations due to changes of osmotic pressure and denaturation of cytoskeleton proteins, unfolding of information-bearing proteins, clumping and precipitation out of solution, tend to be irreversible, many-to-one, transitions.
A neuron for Halle Berry, for example, might respond “to the concept, the abstract entity, of Halle Berry”, and would fire not only for images of Halle Berry, but also to the actual name “Halle Berry”.[15] However, there is no suggestion in that study that only the cell being monitored responded to that concept, nor was it suggested that no other actress would cause that cell to respond (although several other presented images of actresses did not cause it to respond).
That wiki article looks dated. See these two, more recent abstracts: [1], [2].
Anyways, the point isn’t whether there are actual grandmother cells, or “merely” a very small number of cells serving the same purpose. It is that there are crucial brain functions with little to no redundancy.
The brain has redundancy at the level of neurons: it is quite resilient against diffuse neuron loss, and in case of localized damage, unless the affected area is large or includes key regions such as the brainstem, impairment is often limited to one or a few functions, and in some cases it even reorganizes to transfer the lost functions to other areas, partially recovering them.
However, there is no expectation that the brain has redundancy against the loss of an information storage medium that is used in all neurons.
If you destroy half of your collection of DVDs, the information in the other half is still intact. If you destroy every odd-numbered track on all of your DVDs, instead, most of the remaining data will be too fragmentary to be of any use, even if the number of bits you destroyed is the same in both cases.
There can be a lot of redundancy within neurons as well. Just because you find causally relevant chemical densities that predict neuron states doesn’t mean that there aren’t other chemical densities that also predict those same states.
Is there any evidece of such large redundancy at the level of biochemical information storage? I’m not aware of it, and I can’t see a good reason for such thing to have been evolved.
I’m not a neuroscientist, but AFAIK, I’m not sure that talking about chemical densities is the most appropriate way to frame the discourse here: synapses are small enough that the discrete nature of protein complexes and structures becomes relevant. While disrupting a single molecule wouldn’t significantly affect the neuron state, a process that causes generalized misallignment between the active zones on one side and corresponding receptors on the other side, or between the two halves of electric gap junctions, or other widespread distortions, could easily do. Unless this process is reversible in the information-theoretic sense, these bits of information are lost forever.
IIUC, the type of distortions that occur during cryopreservation: membrane deformations due to changes of osmotic pressure and denaturation of cytoskeleton proteins, unfolding of information-bearing proteins, clumping and precipitation out of solution, tend to be irreversible, many-to-one, transitions.
Depends on what axis of resilience (as you alluded to).
For memory, confer grandmother cells.
That wiki article looks dated. See these two, more recent abstracts: [1], [2].
Anyways, the point isn’t whether there are actual grandmother cells, or “merely” a very small number of cells serving the same purpose. It is that there are crucial brain functions with little to no redundancy.