© 2014 Peter Free
Citation — to study
Fabian Fernandez, Derek Lu, Phong Ha, Patricia Costacurta, Renee Chavez, H. Craig Heller, and Norman F. Ruby, Dysrhythmia in the suprachiasmatic nucleus inhibits memory processing, Science 346(6211): 854-857, DOI: 10.1126/science.1259652 (14 November 2014)
Citation — to press release
Bjorn Carey, Stanford biologists explore link between memory deficit and misfiring circadian clock, Stanford University (17 November 2014)
Method and findings
From the abstract:
Chronic circadian dysfunction impairs declarative memory in humans . . . . [H]uman dysrhythmia occurs while SCN [suprachiasmatic nucleus] circuitry is genetically and neurologically intact.
Siberian hamsters (Phodopus sungorus) are particularly well suited for translational studies because they can be made arrhythmic by a one-time photic [light] treatment that severely impairs spatial and recognition memory.
We found that once animals are made arrhythmic, subsequent SCN ablation [destruction] completely rescues memory processing.
© 2014 Fabian Fernandez, Derek Lu, Phong Ha, Patricia Costacurta, Renee Chavez, H. Craig Heller, and Norman F. Ruby, Dysrhythmia in the suprachiasmatic nucleus inhibits memory processing, Science 346(6211): 854-857, DOI: 10.1126/science.1259652 (14 November 2014) (at Abstract) (extracts)
From Bjorn Carey’s excellent press release:
[T]hey trained Siberian hamsters in a standard learning and memory task, which involved familiarizing them with two objects and then, some time later, changing up one of the objects and seeing if the rodents noticed. On the whole, the animals excelled at the test.
Once the animals had mastered the task, the researchers exposed them to light at odd intervals, which threw off their circadian rhythms. The arrhythmic hamsters were then given the same memory task, and failed miserably.
Next, the researchers surgically removed each hamsters’ SCN . . . and gave the memory test a third time . . . . [T]he animals performed the test as well as they had at the beginning of the experiment.
Elderly people with neurodegenerative memory deficiencies also often complain of poor sleep, which can be associated with weakened circadian timing.
The new work suggests that rather than repairing the systems responsible for a misfiring SCN, it might be more productive to simply remove it from the equation.
“The more I investigate it, the idea of shutting off the SCN as a way of restoring memory ability in humans seems more provocative and possibly doable,” Ruby said. “If you are treating a a neurodegenerative brain, rather than fixing the circadian clock, it might be easier to just pharmacologically shut down the SCN.”
© 2014 Bjorn Carey, Stanford biologists explore link between memory deficit and misfiring circadian clock, Stanford University (17 November 2014) (extracts)
Without a gram of belittlement intended, the suprachiasmatic nucleus probably controls a good deal more than we recognize. Taking it out of the “circuit” may create more problems than it solves.
I am also not convinced that there is a substantial subset among the elderly population, who simply have a circadian rhythm problem that is not accompanied by a wider neuro-degenerative one. The latter might itself account for the inability to drag an even adequately formed memory out of storage in useable form.
The moral? — Excellent work and a promising avenue of further investigation
My caveats may be completely wrong and are not intended to slight the worth of this clever study.