Pharmacological enhancement of memory or cognition in normal subjects
Open accessAbstract
The possibility of expanding memory or cognitive capabilities above the levels in high functioning individuals is a topic of intense discussion among scientists and in society at large. The majority of animal studies use behavioral endpoint measures; this has produced valuable information but limited predictability for human outcomes. Accordingly, several groups are pursuing a complementary strategy with treatments targeting synaptic events associated with memory encoding or forebrain network operations. Transcription and translation figure prominently in substrate work directed at enhancement. Notably, the question of why new proteins would be needed for a now-forming memory given that learning-driven synthesis presumably occurred throughout the immediate past has been largely ignored. Despite this conceptual problem, and some controversy, recent studies have reinvigorated the idea that selective gene manipulation is a plausible route to enhancement. Efforts to improve memory by facilitating synaptic encoding of information have also progressed, in part due of breakthroughs on mechanisms that stabilize learning-related, long-term potentiation (LTP). These advances point to a reductionistic hypothesis for a diversity of experimental results on enhancement, and identify under-explored possibilities. Cognitive enhancement remains an elusive goal, in part due to the difficulty of defining the target. The popular view of cognition as a collection of definable computations seems to miss the fluid, integrative process experienced by high functioning individuals. The neurobiological approach obviates these psychological issues to directly test the consequences of improving throughput in networks underlying higher order behaviors. The few relevant studies testing drugs that selectively promote excitatory transmission indicate that it is possible to expand cortical networks engaged by complex tasks and that this is accompanied by capabilities not found in normal animals.
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Enhancing normal learning by judicious pharmacotherapy has recently received attention.
“Indeed, enhancing normal learning by judicious pharmacotherapy has recently received attention111”
From The right time to learn: Mechanisms and optimization of spaced learning (2016) · cites this paper as [111]
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The ultrastructural localization of calcium‐activated protease “calpain” in rat brain
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Self-citationBenzamide-Type AMPA Receptor Modulators Form Two Subfamilies with Distinct Modes of Action
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Self-citationStructural Determinants of d-Cycloserine Efficacy at the NR1/NR2C NMDA Receptors
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Quinoxaline derivatives are high-affinity antagonists of the NMDA receptor-associated glycine sites
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Rats and humans paying attention: Cross-species task development for translational research.
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Long‐term potentiation of monosynaptic EPSPS in rat piroform cortex in vitro
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Self-citationMassed but not spaced training impairs spatial memory
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Self-citationNeuroenhancement: status quo and perspectives
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Integrin Dynamics Produce a Delayed Stage of Long-Term Potentiation and Memory Consolidation
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Developmental and regional differences in the consolidation of long-term potentiation
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Self-citationTargeting of NMDA receptors in the treatment of major depression
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Synaptic tagging and capture in the living rat
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Brief ampakine treatments slow the progression of Huntington's disease phenotypes in R6/2 mice
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Self-citationRegulation of brain neurctrophin expression by physiological activity
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Self-citationBDNF upregulation rescues synaptic plasticity in middle-aged ovariectomized rats
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Self-citationNicotinic Acetylcholine Receptor
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Learning induces neurotrophin signaling at hippocampal synapses
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Self-citationLTP Induction Translocates Cortactin at Distant Synapses in Wild-Type But NotFmr1Knock-Out Mice
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Self-citationDeletion of Ecto-5′-Nucleotidase (CD73) Reveals Direct Action Potential-Dependent Adenosine Release
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7,8-Dihydroxyflavone improves memory consolidation processes in rats and mice
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Glycine site associated with the NMDA receptor modulates long‐term potentiation
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Self-citationEnhanced glutamatergic neurotransmission facilitates classical conditioning in the freely moving rat
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Self-citationMaintenance of long-term memory storage is dependent on late posttraining Egr-1 expression
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Neuronal Rac1 Is Required for Learning-Evoked Neurogenesis
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Synaptic Abnormalities in the Infralimbic Cortex of a Model of Congenital Depression
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Self-citationThe substrate for long-lasting memory: If not protein synthesis, then what?
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Self-citationCholinomimetics induce θ rhythm and reduce hippocampal pyramidal cell excitability
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Human Cortical θ during Free Exploration Encodes Space and Predicts Subsequent Memory
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Self-citationMechanism based approaches for rescuing and enhancing cognition
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Self-citationThe generation of theta rhythm in hippocampal formation maintainedin vitro
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Self-citationNeuronal Categorization and Discrimination of Social Behaviors in Primate Prefrontal Cortex
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The right time to learn: Mechanisms and optimization of spaced learning
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- Authors
- Lynch, G.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Lynch, Gary
- ORCID
- Lynch, Gary
- Venue
- Frontiers in Systems Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2014
- Volume
- 8
- Pages
- 90-90
- ISSN
- 1662-5137 (ISSN-L)
- PMC
- PMC4033242
- OpenAlex
- W2110892837
- Cited by
- 46
- References
- 168
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 4 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 5 · 2015: 7 · 2014: 3
- FWCI
- 0.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Systems Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- National Science Foundation (1146708)
- University of California, Irvine
- Office of Naval Research
- National Institute of Neurological Disorders and Stroke (P01NS045260, NS045260)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neuroethics, Human Enhancement, Biomedical Innovations
- Keywords
- cognitive enhancement, memory enhancement, synaptic plasticity, long-term potentiation, genetic engineering, transcription and translation, excitatory synaptic transmission, cortical networks, learning
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