Consider the following abstracts about intervention to improve memory, one real, and one fictitious:
Memory enhancement in healthy older adults using a brain plasticity-based training program: A randomized, controlled study
Mahncke HW et al. PNAS August 15, 2006 vol. 103 no. 33 12523-12528
Normal aging is associated with progressive functional losses in perception, cognition, and memory. Although the root causes of age-related cognitive decline are incompletely understood, psychophysical and neuropsychological evidence suggests that a significant contribution stems from poorer signal-to-noise conditions and down-regulated neuromodulatory system function in older brains. Because the brain retains a lifelong capacity for plasticity and adaptive reorganization, dimensions of negative reorganization should be at least partially reversible through the use of an appropriately designed training program. We report here results from such a training program targeting age-related cognitive decline. Data from a randomized, controlled trial using standardized measures of neuropsychological function as outcomes are presented. Significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25) were documented in the group using the training program. Memory enhancement appeared to be sustained after a 3- month no-contact follow-up period. Matched active control and no-contact control groups showed no significant change in memory function after training or at the 3-month follow-up. This study demonstrates that intensive, plasticity-engaging training can result in an enhancement of cognitive function in normal mature adults.
Memory enhancement in healthy older adults using genetic modification also protects against Alzheimerâs Disease.1
I M Genius, Prestigious Journal 1 (1): 1-10
Inserting extra copies of the gene NR2B, which encodes the NMDA receptor, leads to improved memory and also prevents onset of Alzheimerâs Disease. Two chemical signals are needed to trigger this nerve cell receptor, which means that it plays a key role in forming associations. For instance, if you touch a flame, the visual signal and pain signal arrive to the brain at roughly the same time, activating NMDA receptors and creating a memory. Healthy adults were given extra copies of the gene and these were rigged so that genesâ activity would increase over time as the adults aged. Earlier studies had revealed that in young animals, NMDA receptors are activated even by signals that arrive somewhat far apart, facilitating learning. As an animal ages, though, the signals must travel more in step to trip NMDA receptors and cement memories. Adults treated with the NR2B gene had significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25). In addition, adults treated with the genes showed lower levels of onset of Alzheimerâs Disease compared with matched controls.
For discussion
Are these interventions therapy or enhancement? (Is age-related loss of memory a disease?)
Are there morally significant differences between the methods (cognitive training versus genetic
modification)?
What are the potential harms and benefits from using these interventions?
What are your views on the moral permissibility of the interventions?
How would your responses change if the interventions were for increasing muscle mass and performance in elite athletes?
Consider the following abstracts about intervention to improve memory, one real, and one fictitious:
Memory enhancement in healthy older adults using a brain plasticity-based training program: A randomized, controlled study
Mahncke HW et al. PNAS August 15, 2006 vol. 103 no. 33 12523-12528
Normal aging is associated with progressive functional losses in perception, cognition, and memory. Although the root causes of age-related cognitive decline are incompletely understood, psychophysical and neuropsychological evidence suggests that a significant contribution stems from poorer signal-to-noise conditions and down-regulated neuromodulatory system function in older brains. Because the brain retains a lifelong capacity for plasticity and adaptive reorganization, dimensions of negative reorganization should be at least partially reversible through the use of an appropriately designed training program. We report here results from such a training program targeting age-related cognitive decline. Data from a randomized, controlled trial using standardized measures of neuropsychological function as outcomes are presented. Significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25) were documented in the group using the training program. Memory enhancement appeared to be sustained after a 3- month no-contact follow-up period. Matched active control and no-contact control groups showed no significant change in memory function after training or at the 3-month follow-up. This study demonstrates that intensive, plasticity-engaging training can result in an enhancement of cognitive function in normal mature adults.
Memory enhancement in healthy older adults using genetic modification also protects against Alzheimerâs Disease.1
I M Genius, Prestigious Journal 1 (1): 1-10
Inserting extra copies of the gene NR2B, which encodes the NMDA receptor, leads to improved memory and also prevents onset of Alzheimerâs Disease. Two chemical signals are needed to trigger this nerve cell receptor, which means that it plays a key role in forming associations. For instance, if you touch a flame, the visual signal and pain signal arrive to the brain at roughly the same time, activating NMDA receptors and creating a memory. Healthy adults were given extra copies of the gene and these were rigged so that genesâ activity would increase over time as the adults aged. Earlier studies had revealed that in young animals, NMDA receptors are activated even by signals that arrive somewhat far apart, facilitating learning. As an animal ages, though, the signals must travel more in step to trip NMDA receptors and cement memories. Adults treated with the NR2B gene had significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25). In addition, adults treated with the genes showed lower levels of onset of Alzheimerâs Disease compared with matched controls.
For discussion
Are these interventions therapy or enhancement? (Is age-related loss of memory a disease?)
Are there morally significant differences between the methods (cognitive training versus genetic
modification)?
What are the potential harms and benefits from using these interventions?
What are your views on the moral permissibility of the interventions?
How would your responses change if the interventions were for increasing muscle mass and performance in elite athletes?
