Researchers may finally have uncovered the brain mechanism for storage of long term memories. It's long been suspected that synaptic connections between neurons were part of the mechanism. But somehow our memories survive while individual neurons die and are replaced. There's a new paper on the subject by Travis J. A. Craddock, Jack A. Tuszynski, and Stuart Hameroff, titled "Cytoskeletal Signaling: Is Memory Encoded in Microtubule Lattices by CaMKII Phosphorylation?" The researchers describe complex electrostatic interactions between CaMKII, tubulin protein compounds, and microtubule protein structures inside the neurons. It turns out this may be the process used to read and write long term memories into an information storage lattice, as well as perform a variety of biocomputation based on traditional logical operations such as AND, XOR, NOT, and OR. The researchers summarize their discoveries this way:
"We demonstrate a feasible and robust mechanism for encoding synaptic information into structural and energetic changes of microtubule (MT) lattices by calcium-activated CaMKII phosphorylation. We suggest such encoded information engages in ongoing MT information processes supporting cognition and behavior, possibly by generating scale-free interference patterns via reaction-diffusion or other mechanisms. As MTs and CaMKII are widely distributed in eukaryotic cells, the hexagonal bytes and trytes suggested here may reflect a real-time biomolecular information code akin to the genetic code."
There are several theories about the low-level structures. Each storage lattice could be binary or trinary and store as little as 64 bits or as much as 5281 unique states. The article includes estimates of the brain's energy consumption rate for various data encoding rates. This new research suggests current neural network models may be woefully inadequate for artificial intelligence. In addition to implications for AI, the research suggests possible routes toward improving and even repairing memory function in human brains suffering from neuro-degenerative diseases such as Alheimer's. For more see the University of Alberta news release.