First of all, I would like to praise the hard work of Roy and other authors. By definition, however, early AD is the clinical condition that arises after MCI, where tauopathy and neurodegeneration had already started. So the models that the authors used in this study are not models of early AD. Another model used, the 3XAD mice, are not even a model of AD because the tau mutation used causes FTDP-17, not AD.
Bateman and colleagues, 2012, showed that a minor cognitive decline starts after Aβ deposition approximately 10 years before clinical AD onset in humans. So, Roy's finding may account for this preclinical minor cognitive decline, but contextual fear conditioning would be very hard even for humans under these conditions to forget. Twenty-four hours is equally 24 hours for mice and for humans, in my view.
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RIKEN Center for Brain Science
First of all, I would like to praise the hard work of Roy and other authors. By definition, however, early AD is the clinical condition that arises after MCI, where tauopathy and neurodegeneration had already started. So the models that the authors used in this study are not models of early AD. Another model used, the 3XAD mice, are not even a model of AD because the tau mutation used causes FTDP-17, not AD.
Bateman and colleagues, 2012, showed that a minor cognitive decline starts after Aβ deposition approximately 10 years before clinical AD onset in humans. So, Roy's finding may account for this preclinical minor cognitive decline, but contextual fear conditioning would be very hard even for humans under these conditions to forget. Twenty-four hours is equally 24 hours for mice and for humans, in my view.
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