How Does Human Memory Work?

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How do molecules organize to define one memory from another? Why does it appear like any sensory input searches for an interpretation fit or match, initially or finally? What makes any memory intelligent? Why can the memory of something become the basis for caution—or action—against something else? How do some memories last while others fade? Are there differences between the molecules that arrange what a memory is from those that make it permanent? \n

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There are two defining elements in the brain in several memory studies, the gene of a molecule and the molecule. If the gene is expressed—for the availability of the molecule—then the memory would work, so to speak. \n

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Now, if some conceptual architecture of memory were to be developed, would it be predicated on the gene or on the molecule? It is theorized that genes—like neurons—are hosts, while molecules mechanize. Simply, neurons and genes would have to be present for the molecule to be available, but it is the molecule that makes memories possible. It is like a house and the facilities in it that are useful to people. \n

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This means that in exploring the basis of human memory, molecules are ahead of genes and neurons, conceptually. Every synapse, strong or weak, has molecules at the cleft. It is theorized that the formation of these molecules differently, in a set, in a cluster of neurons, specifies one memory from the next. Simply, synapses can be described as provision pulleys, but it is the configuration of molecules that define memory. \n

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There are several so-called memory molecules, WWC1 [or KIBRA], PKC iota/lambda[PKCι/λ], CaMKII, PKMzeta [PKMζ], cGMP/PKG, cAMP, PKA, CRE, CREB-1, CREB-2, CPEB and so forth. The question is to explore what molecules structure memory and what molecules make them last. \n

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It is known that for some memories to last, repetition often is necessary. Also, consequences may ensure that long-term caution is applied. Then there could be a parallel event, say some trauma or something else that could make the memory last. There could also be an understanding of it. \n

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There is a recent paper in Science, KIBRA anchoring the action of PKMζ maintains the persistence of memory, stating that, "How can short-lived molecules selectively maintain the potentiation of activated synapses to sustain long-term memory? Here, we find kidney and brain expressed adaptor protein (KIBRA), a postsynaptic scaffolding protein genetically linked to human memory performance, complexes with protein kinase Mzeta (PKMζ), anchoring the kinase’s potentiating action to maintain late-phase long-term potentiation (late-LTP) at activated synapses. Two structurally distinct antagonists of KIBRA-PKMζ dimerization disrupt established late-LTP and long-term spatial memory, yet neither measurably affects basal synaptic transmission. Neither antagonist affects PKMζ-independent LTP or memory that are maintained by compensating PKCs in ζ-knockout mice; thus, both agents require PKMζ for their effect. KIBRA-PKMζ complexes maintain 1-month-old memory despite PKMζ turnover. Therefore, it is not PKMζ alone, nor KIBRA alone, but the continual interaction between the two that maintains late-LTP and long-term memory." \n

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If KIBRA and PKMζ have to interact to result in long-term memory, what provenance of long-term memory might this be? Repetition, consequence, parallel event of something, or an understanding of a situation? \n

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It is unlikely that molecules for memory permanence and memory configuration are totally independent because the first thing is often the form of memory before it can be permanent or temporal. \n

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For example, cars, doors, windows, shoes, books, devices, and so forth have different types, and the memory interprets all. The memory does not store all cars separately, but it often collects what is common between two or more then groups them into what can be called a thick set. It is this thick set that may become a permanent basis for the interpretation of similar memories, conceptually. \n

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So the question is how do thick sets work? Then for thin sets—where the most unique information is stored—it is likely to be temporal since specific things about every door are hardly remembered, but those of doors are often known and remembered. \n

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Molecules in formation mechanize memories, conceptually. Their placement of the memory may decide if permanent molecules may act on them, conceptually. It is the opening by formation [or configuration] molecules that may allow others to act, conceptually. \n

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There is also the role of relays from one part of the thick set to the next, or one part of the memory to the other by electrical signals that may also determine allowance of permanent molecules, conceptually. It is theorized that electrical signals in a set strike at chemical signals, to fit or match what might be available for interpretation, initially or finally. Possibility for initial and final interaction is because electrical signals split, in a set, with some going ahead of others, conceptually. \n

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Research in cellular and molecular neuroscience is necessary for neuropharmacology. However, theoretical neuroscience may lead the way to shape how to place studies as they emerge for perpendicular options against mind problems. \n

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There is a recent paper in Nature, Competitive processes shape multi-synapse plasticity along dendritic segments, stating that, "Neurons receive thousands of inputs onto their dendritic arbour, where individual synapses undergo activity-dependent plasticity. Long-lasting changes in postsynaptic strengths correlate with changes in spine head volume. The magnitude and direction of such structural plasticity - potentiation (sLTP) and depression (sLTD) - depend upon the number and spatial distribution of stimulated synapses. However, how neurons allocate resources to implement synaptic strength changes across space and time amongst neighbouring synapses remains unclear. Here we combined experimental and modelling approaches to explore the elementary processes underlying multi-spine plasticity. We used glutamate uncaging to induce sLTP at varying number of synapses sharing the same dendritic branch, and we built a model incorporating a dual role Ca2+-dependent component that induces spine growth or shrinkage. Our results suggest that competition among spines for molecular resources is a key driver of multi-spine plasticity and that spatial distance between simultaneously stimulated spines impacts the resulting spine dynamics." \n

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There is another recent paper in Nature, Images with harder-to-reconstruct visual representations leave stronger memory traces, stating that, "Much of what we remember is not because of intentional selection, but simply a by-product of perceiving. This raises a foundational question about the architecture of the mind: how does perception interface with and influence memory? Here, inspired by a classic proposal relating perceptual processing to memory durability, the level-of-processing theory, we present a sparse coding model for compressing feature embeddings of images and show that the reconstruction residuals from this model predict how well images are encoded into memory. In an open memorability dataset of scene images, we show that reconstruction error not only explains memory accuracy, but also response latencies during retrieval, subsuming, in the latter case, all of the variance explained by powerful vision-only models. We also confirm a prediction of this account with ‘model-driven psychophysics’. This work establishes reconstruction error as an important signal interfacing perception and memory, possibly through adaptive modulation of perceptual processing."

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