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Cognitive Enhancement

Cognitive Enhancement. By Group 11: Steve, Natalie, Mayank. What is Cognitive Enhancement?. Aspects of Cognition Perception, attention, understanding, memory Types of intervention Therapeutic to repair dysfunction Enhancement intervention in some way other than repairing a dysfunction.

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Cognitive Enhancement

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  1. Cognitive Enhancement By Group 11: Steve, Natalie, Mayank

  2. What is Cognitive Enhancement? • Aspects of Cognition • Perception, attention, understanding, memory • Types of intervention • Therapeutic • to repair dysfunction • Enhancement • intervention in some way other than repairing a dysfunction

  3. Normal and Deficit Use • Deficit and Normal use inseparable • Cognitive Enhancement -positive change in cognitive skills or abilities

  4. Prescription or “Natural” • Prescription enhancers viewed as “cheating” • Beyond natural human endowment • Herbal remedies perceived as natural enhancement • within the bounds of self improvement

  5. Attention and Arousal • Difference between arousal and attention • Caffeine –arousal • Ritalin- attention • Mainly stimulants

  6. Caffeine • Found in coffee bean and cola nut • History • In use since stone age • Effects • Reaction time • prevents deterioration • flat dose response • prevents boredom

  7. Ritalin • Use • Treatment of ADHD • Nonprescription use among college students • History • 1st synthesized in 1940 • Effects • Narrowing of attentional spotlight • Excitation of inhibitory neurotransmitter

  8. Memory • Demand for memory improving products • Prevalence of Ahlzimer’s • Ginkgo Biloba • Uniqueness of self in memory • Less adverse effects

  9. Memory: Mechanistic Details • Overview • Memory as a function of consciousness • LTP • Short-term potentiation • Early LTP • Induction • Maintenance • Late LTP • Expression • Cognitive Enhancement Drugs: Memory

  10. Memory and Consciousness • Memory is our ability to be able to retain and recall past experiences • Initiation occurs in the hippocampus, storage is considered to be distributed arbitrarily across the frontal cortical regions (Kemp et al. 2007) • Usually broken down into declarative (explicit) and procedural (implicit)(Wikipedia: Memory, 2007) • LTP is the main basis for memory initiation and consolidation

  11. LTP • Long term potentiation • Utilizes glutamatergic synaptic transmission • AMPA and NMDA receptor mediated(Lisman et al., 2006) • Glutamatergic release modulates genetic transcription factors such as CREB through a second messenger system, primarily involving cAMP and PKA • LTP involves three phases • Short-term phase • Early phase • Late phase • Early and Late phase • Broken down into: induction, maintenance, and expression • Hebbian Synaptic Plasticity Images Courtesy of: Mann, 2004

  12. Short-term Potentiation • AMPA receptor mediation is required for LTP induction(Sweatt, 1999) • AMPA receptors are excited on moment-to-moment activity • EPSP, or excitatory postsynaptic potential, is a measure of the amount of electrical signal that results from the activity of the aforementioned receptors • Magnitude and frequency are the main players in LTP: high frequency of EPSPs with sufficient electrical output are needed(Sweatt, 1999) • Subsequent electrical stimuli need to give enough of electrical signals to prevent a previous EPSP response from dying(Sweatt, 1999)

  13. Early LTP • E-LTP, a protein synthesis-independent pathway • This phase of LTP is where the high frequency and sufficient electrical stimulus result in temporary changes to pre- and post-synaptic elements • Not sure what causes E-LTP to lead to L-LTP (Late LTP) • Insertion of AMPA receptors or increase in glutamatergic response(Wikipedia: Long-term Potentiation, 2007) • Downstream cascading molecular events involve calmoldulin/calcium-dependent protein kinase II (CaMKII), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), and tyrosine kinases(Lledo et al., 1995), (Sweatt, 1999)

  14. Late LTP • L-LTP, an exceedingly protein dependent pathway of potentiation • Hebbian Synaptic Plasticity(Sweatt, 1999) • The formation of new synapses in response to a repetitive and significant event/stimulus to certain neuronal cells • Two phase system: protein synthesis occurs then protein synthesis with transcription modulation • Calmoldulin/calcium-independent protein kinase IV (CaMKIV) and cAMP response element binding protein (CREB) are two significant players in L-LTP(Sweatt, 1999) • Protein Kinase A (PKA) activates second messenger system that involves cyclic adenosine monophosphate (cAMP) • cAMP reacts to CREB modulating transcription factors and inducing protein synthesis that effectively results in the creation of new synapses Images Courtesy of: Mann, 2004

  15. Ampakines • Increase attention span, alertness, and memory. • Lack side effects of many traditional stimulants. • Potential treatment for Alzheimers, Parkinsons’s, and other neurodegenerative diseases. • Could also treat normal age related deficits, or even augment the mental faculties of healthy individuals

  16. Mechanism • Ampakines work by allosterically binding AMPA-type glutamate receptors. • Facilitate glutamatergic signaling • Increase levels of trophic factors BDNF. • This promotes plasticity at the synapse, which could translate into better cognitive performance.

  17. Synaptic Mechanism • Potentiate induction of LTP, • by facilitating AMPA mediated • depolarization. • Allows endogenously released • glutamate to bind AMPA • and NMDA receptors. Lynch (2000)

  18. CX-516 Increases Recall • 24 subjects ages 65-76 • tested on recall of nonsense syllables after delay • Increased performance seen 75 min after ingestion • Greatest increase seen in 900 mg group • Dosage dependent increase in recall ability Lynch (1997)

  19. CX- 727 • Hippocampal slices exposed to neurotoxic • TMT for 4 hrs • Treated with different levels of CX 727 for • 24 hrs after exposure. • Slices exposed to higher dosage showed • highest optical density for AMPA receptor • subunit GluR. • Dose dependent neuroprotection. Munirathinam (2002)

  20. Altered State? SUPER NORMAL ? • Yes. By increasing mental faculties • above “normal,” Ampakines and other • such drugs produce altered states. • Cognitive enhancement may have far • reaching social implications and raises • serious ethical questions. Normal Relief From Anxiety Disinhibition Sedation Hypnosis General anesthesia Coma Death

  21. Bibliographic References • Kemp A, & Manahan-Vaughan D. Hippocampal long-term depression: master or minion in declarative memory processes?. Trends in Neurosciences. 2007; 30(3):111-8. • Mann MD. Learning and Memory. May 17, 2004, at 20:57 UTC. The Nervous System in Action. Available at: http://www.unmc.edu/Physiology/Mann/mann19.html. Accessed June 5, 2007. • Lisman J, & Raghavachari S. A unified model of the presynaptic and postsynaptic changes during LTP at CA1 synapses. Science. 2006; 2006(356) • Lledo PM, Hjelmstad GO, Mukherji S, Soderling TR, Malenka RC, et al. Calcium/calmodulin-dependent kinase II and long-term potentiation enhance synaptic transmission by the same mechanism. Proceedings of the National Academy of Sciences of the United States of America. 1995; 92(24):11175-9. • Lynch, G., Granger, R., Ambros-Ingerson, J., Davis, C.M., Kessler, M., Schehr, R. (1997). Evidence That a Positive Modulator of AMPA-Type Glutamate Receptors Improves Delayed Recall in Aged Humans. Experimental Neurology, 145, 89–92. • Lynch, G. (2002). Memory enhancement: the search for mechanism-based drugs. Neuroscience, 5, 1035-1038.

  22. References (cont) • Sweatt JD. Toward a molecular explanation for long-term potentiation. Learning & memory. 1999; 6(5):399-416. • Wikipedia contributors. Memory. Wikipedia, The Free Encyclopedia. June 5, 2007, at 22:36 UTC. Available at: http://http://en.wikipedia.org/wiki/Memory. Accessed June 5, 2007. • Wikipedia contributors. Long-Term Potentiation. Wikipedia, The Free Encyclopedia. May 23, 2007, at 23:42 UTC. Available at: http://en.wikipedia.org/wiki/Long-term_potentiation. Accessed June 5, 2007. • Bostrom, Nick, and Sandberg, Anders. “Cognitive Enhancement :Methods, Ethics, Regulatory Challenges." Science and Engineering Ethics, 2007. • Smit, H.J., and Rogers, P.J. “Effects of Low Does of Caffeine on Cognitive Performance , mood and thirst in low and high Consumers.” Pharmacology. 28 July 2000. • Carroll, Bronwen C., et al. ”Patterns and Knowledge of Nonmedical Use of Stimulants Among College Students.” Arch Pediatrics and Adolescent Medicine. Vol 160, May 2007. • Munirathinam,S., Rogers, G., Bahr, B.A. (2002) Positive Modulation of _-imino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid-Type Glutamate Receptors Elicits Neuroprotection after Trimethyltin Exposure in hippocampus. Toxicology and Applied Pharmacology,185, 111–118

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