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Dr. Jack Tuszynski, University of Alberta – Neurobiology of Memory Storage

In today’s Academic Minute, Dr. Jack Tuszynski of the University of Alberta explores the physical process that allows the brain to store and retrieve memories.

Jack Tuszynski is Allard Chair and Professor of Experimental Oncology at the University of Alberta where his research interests are strongly linked to the protein tubulin and the microtubules assembled from it. He holds a Ph.D. in condensed matter physics from the University of Calgary.

About Dr. Tuszynski

Dr. Jack Tuszynski – Neurobiology of Memory Storage

The molecular mechanism of memory formation is a major unsolved scientific puzzle with great implications for health and disease. Memory is understood to depend on synaptic connections among brain neurons and channel activity involving neural network pathways. While synaptic components are short-lived and frequently re-cycled, memories last lifetimes which suggests that synaptic information and memory are encoded at a deep molecular level, much like the genetic code in DNA. With my former student Travis Craddock and  research colleague Dr. Stuart Hameroff we postulated a plausible mechanism for encoding synaptic memory at a subcellular level, namely in microtubules, which are major components of the neuronal cytoskeleton. Microtubules are cylindrical polymers composed of ‘tubulin’ protein. They play numerous roles in cells including neuronal growth, synaptic regulation, transport and cell division.

Currently, the best experimental model for neuronal memory involves so-called long term potentiation. This means that pre-synaptic excitation causes long-lasting post-synaptic sensitivity in communicating neurons. The key molecular player in this process is an enzyme called calcium/calmodulin-dependent protein kinase II,  (CaMKII for short). Calcium ions entering post-synaptic neurons activate this enzyme and cause it to deposit phosphate groups,  which is called phosphorylation.Each such event encodes one ‘bit’ of information.  Each CaMKIIA single enzyme can encode six6 bits of information in a microtubule which we showed using precise molecular modeling. With many billions of neurons in the brain, this would result in an enormous information storage capacity well exceeding the most powerful supercomputers available today at extremely low energy cost. This  mechanism explains how microtubules can influence axonal firings, regulate synapses, affect differentiation and various functions of cells. This could provide a real-time, interactive biological code in contrast to the static genetic information stored in DNA. Decoding and interfacing to microtubule bits could enable therapeutic intervention in pathological processes, such as Alzheimer’s disease in which microtubule disruption plays a key role, and brain injury in which microtubules can repair and regenerate neurons and synapses.

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