Authors: Gerard Marx, Chaim Gilon
What lies between the vital physiology and pathology of cognitive aging?
To comprehend the brain’s mental function and dysfunction, we focus on memory, its formation and loss. Our expanded tripartite mechanism of memory involves the following compartments: Stimulated brain cells (neurons + glial cells) which secrete dopants (>10 metals and >80 neuro-transmitters (NTs) and glio-transmitters (GTs)) into the extracellular matrix (nECM/PNN) enveloping all brain cells, that performs as a “memory material”. The metal-centered complexes formed within the nECM/PNN are molecular correlates of cognitive units of information (cuinfo) that encode experience. The transmitters (NTs+GTs) embody emotive quality that elicit physiologic reactions from organs and glands to encode emotive states. As for decoding the cuinfo, aggregates (mosaics) of sensors (GPCR- and K-channel family proteins) within the lipid-bilayer comprising the cell membranes are capable of “reading” and integrating the cuinfo, transliterating them into an experiential mental state.
As to memory loss, aside from gross injuries or anatomical abnormalities, we look to molecular-level decay, which involve processes such as Toxicity or deficiency of trace metals, degradation of the nECM/PNN or it’s by enzymatic or redox (Fenton) reactions, uncontrolled lipid peroxidation (i.e. endocannabinoids) or autoimmune antibodies (i.e. anti- metallothionein) or lysozyme amyloid fibril formation. Interference with the optimal operation of the expanded tripartite mechanism of emotive memory is reflected by clinical features of memory loss in patients with degenerative disorders.
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