Scientific American published a web feature on the 3rd summarizing 5 years of neuroimmunological research. Before 2003 the brain was considered off-limits to the immune system due to the exclusivity of the blood-brain barrier. Princeton researchers were shocked to discover C1q, a gene that codes for a family of proteins responsible for the recognition of pathogens, while searching for genes that respond to neuronal firing.

The discovery opened up a variety of research avenues. We now know that the proteins rest on the surface of neurons, play a role in the plasticity of synaptic connections, and have a developmental role in pruning unneeded connections.

Neuroimmunological dysfunction may also be tied to diseases like glaucoma, schizophrenia, and autism. The development of schizophrenia, particularly, has historically correlated with prenatal infection. Developmental infections like these may detrimentally “distract” the pruning proteins.

Studies like this give me appreciation of how far Markram’s Blue Brain project has to go. It seems relatively simple to summate the chemical inputs and outputs as they relate to the firing of action potentials. Indeed, the current project only seeks to functionally mimic a very specific chunk of rat cortex. But even if they succeeded in modeling the entire rodent brain… phenomena like distractable pruning proteins would add ineffable complexity.

The brain never was and never will be a mere series of inputs and outputs. Much as genes are controlled by the environment that encapsulates them, so too is the brain. If that’s the case, and I suspect it is, the creation of a functional electronic cognizance, an iBrain, seems much farther away.


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