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The ethics of using brain-boosting drugs

Corie Lok

Wednesday, 19 Dec 2007 18:46 UTC

There’s a new forum discussion topic here on Nature Network you might be interested in.

It’s about whether healthy and sick individuals should take drugs to enhance cognition, memory, etc. The discussion stems from a commentary published in this week’s Nature by two Cambridge University researchers.

Have a look and post your comments there.

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    • Sorry, I apologize for writing Ari instead of Avi.

      I don´t know whether the following may be helpful: I´ve read your claim for a paradigm shift and for a new way to think about mental orders.
      I do not believe that ADD will be apparent at the neural network level but I hypothesize that this assumption applies to mental disorders like agnosia.

    • Dear Elisabeth:

      As I understand your explanation, “functional” people are those who jump from the stimulus to a (subjectively defined) goal, without representing the means to achieve it. “Predicative” people are those who analyse the stimulus (e.g. Kanisza illusory triangle) and report their representation of it, only relating it to a goal if they are asked to make such a connection.
      In the current paradigm of executive functions in cognitive neuroscience, “functional” people are at risk of being classified as having a prefrontal function disorder.
      Maybe in a different context (e.g. in the future of our own society) the “functional” behavior turns out to be adaptive, but at this moment they constitute a problem for the educational system. Possibly the whole system is built on sand. However, for those (like me) who work in this context, “functional” students are often “disfunctional” in the sense that they do not play the game we would like them to play.
      Possibly this kind of behavioral tendency is based on prefrontal neural network properties, as proposed by Avi. Experimental data on this regard would be helpful.

      Best,

      Alfredo

    • Dear Alfredo,

      Alfredo: However, for those (like me) who work in this context, “functional” students are often “disfunctional” in the sense that they do not play the game we would like them to play.

      Elisabeth: This description will fit.:-)

      For experimental data see:
      Mölle,M., Schwank, I., Marshall, L., Klöhn, A.,& Born, J.(2000): Dimensional complexitiy and power spectral measures of the EEG during functional versus predicative problem solving. Brain & Cognition, Vol.22 No.3, 547-563

      Schwank, I.: Analysis of Eye-Movement During Functional versus Predicative Problem Solving. 2nd Conference of the European Society for Research in Mathematics Education 24th – 27th Feb. 2001, Marinske Lazne
      http://www.ikm.uni-osnabrueck.de/mitglieder/schwank/schwank_e/schwank_e.html

      Best regards,
      Elisabeth

    • News about Ritalin and Prefrontal Function.
      From ScienceDaily
      Thanks to Malcolm Dean for forwarding it to me.
      Alfredo

      University of Wisconsin-Madison (2008, June 25). How Ritalin Works In
      Brain To Boost Cognition, Focus Attention.

      ScienceDaily (June 25, 2008) — Stimulant medications such as Ritalin
      have been prescribed for decades to treat attention deficit
      hyperactivity disorder (ADHD), and their popularity as “cognition
      enhancers” has recently surged among the healthy, as well. What’s now
      starting to catch up is knowledge of what these drugs actually do in
      the brain. In a paper publishing online this week in Biological
      Psychiatry, University of Wisconsin-Madison psychology researchers
      David Devilbiss and Craig Berridge report that Ritalin fine-tunes the
      functioning of neurons in the prefrontal cortex (PFC) – a brain region
      involved in attention, decision-making and impulse control – while
      having few effects outside it.

      Because of the potential for addiction and abuse, controversy has
      swirled for years around the use of stimulants to treat ADHD,
      especially in children. By helping pinpoint Ritalin’s action in the
      brain, the study should give drug developers a better road map to
      follow as they search for safer alternatives. At the same time, the
      results support the idea that today’s ADHD drugs may be safer than
      people think, says Berridge. Mounting behavioral and neurochemical
      evidence suggests that clinically relevant doses of Ritalin primarily
      target the PFC, without affecting brain centers linked to over-arousal
      and addiction. In other words, Ritalin at low doses doesn’t appear to
      act like a stimulant at all.

      “It’s the higher doses of these drugs that are normally associated
      with their effects as stimulants, those that increase locomotor
      activity, impair cognition and target neurotransmitters all over the
      brain,” says Berridge. “These lower doses are diametrically opposed to
      that. Instead, they help the PFC better do what it’s supposed to do.”

      A behavioral disorder marked by hyperactivity, impulsivity and the
      inability to concentrate, ADHD has been treated for more than a
      half-century with Ritalin, Adderall and other stimulant drugs. New
      reports also indicate these meds have lately been embraced by healthy
      Americans of all ages as a means to boost mental performance.

      Yet, despite their prevalence, we know remarkably little about how
      these drugs work, especially at lower doses that have been proven
      clinically to calm behavior and focus attention in ADHD patients, says
      Berridge. In 2006, his team reported that therapeutic doses of Ritalin
      boosted neurotransmitter levels primarily in the PFC, suggesting a
      selective targeting of this region of the brain. Since then, he and
      Devilbiss have focused on how Ritalin acts on PFC neurons to enhance
      cognition.

      To answer this, the pair studied PFC neurons in rats under a variety
      of Ritalin doses, including one that improved the animals’ performance
      in a working memory task of the type that ADHD patients have trouble
      completing. Using a sophisticated new system for monitoring many
      neurons at once through a set of microelectrodes, the scientists
      observed both the random, spontaneous firings of PFC neurons and their
      response to stimulation of an important pathway into the PFC, the
      hippocampus.

      Much like tiny microphones, the electrodes record a pop every time a
      neuron fires, Devilbiss explains. Analyzing the complex patterns of
      “voices” that emerge is challenging but also powerful, because it
      allows study of neurons on many levels.

      “Similar to listening to a choir, you can understand the music by
      listening to individual voices,” says Devilbiss, “or you can listen to
      the interplay between the voices of the ensemble and how the different
      voices combine.”

      When they listened to individual PFC neurons, the scientists found
      that while cognition-enhancing doses of Ritalin had little effect on
      spontaneous activity, the neurons’ sensitivity to signals coming from
      the hippocampus increased dramatically. Under higher, stimulatory
      doses, on the other hand, PFC neurons stopped responding to incoming
      information.

      “This suggests that the therapeutic effects of Ritalin likely stem
      from this fine-tuning of PFC sensitivity,” says Berridge. “You’re
      improving the ability of these neurons to respond to behaviorally
      relevant signals, and that translates into better cognition, attention
      and working memory.” Higher doses associated with drug abuse and
      cognitive impairment, in contrast, impair functioning of the PFC.

      More intriguing still were the results that came from tuning into the
      entire chorus of neurons at once. When groups of neurons were already
      “singing” together strongly, Ritalin reinforced this coordinated
      activity. At the same time, the drug weakened activity that wasn’t
      well coordinated to begin with. All of this suggests that Ritalin
      strengthens dominant and important signals within the PFC, while
      lessening weaker signals that may act as distractors, says Berridge.

      “These results show a new level of action for cognition-enhancing
      doses of Ritalin that couldn’t have been predicted from single neuron
      analyses,” he says. “So, if you’re searching for drugs that might
      replace Ritalin, this is one effect you could potentially look for.”

      He and Devilbiss also hope the research will help unravel an even
      deeper mystery: exactly how neurons encode complex behavior and
      cognition.

      “Most studies look at how something that impairs cognition affects PFC
      neurons. But to really understand how neurons encode cognitive
      function, you want to see what neurons do when cognition is improved,”
      says Berridge. “So this work sets the stage for examining the
      interplay among PFC neurons, higher cognition, and the action of
      therapeutic drugs.”

      The work was funded by the National Institute on Drug Abuse, the
      National Institute of Mental Health and the UW-Madison Discovery Seed
      Grant Program.

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