While the Petersen criterion for cognitive impairment is a score 1.5 standard deviations away from normal values on neuropsychological tests, however, Acosta-Baena and colleagues defined impairment as 2 standard deviations away. They chose this more stringent selleck products cut-off value to reduce the possibility of false positives; a valid justification, although it limits how comparable their results are with studies employing the Petersen criteria. Comparability within the field is further limited by the fact that many other studies do not incorporate neuropsychological results into their classification of MCI, instead defining it as a score of 0.5 on the clinical dementia rating scale; a structured interview with the participant and a close informant [7].
As the field moves forward and prevention trials for familial AD are launched, it will be crucial that different studies share a common construct of MCI if the efficacies of different therapies are to be compared. The situation is more complex regarding the term pre-MCI, which is conventionally used to describe subjective memory complaints without evidence of neuropsychological deficit [8]. Acosta-Baena and colleagues, however, use the term pre-MCI for individuals with objective cognitive impairment who are either asymptomatic or symptomatic with a score on the subjective memory complaints checklist lower than the noncarrier mean. In some centres this symptomatic pre-MCI group would have been classified as MCI, and the findings by the authors of some transient recovery in the symptomatic pre-MCI group may be akin to the subset of MCI patients in other studies whose symptoms revert.
The authors speculate that cognitive reserve is the source of the transient recovery in these individuals; although an alternative explanation may be that anxiety or depression was the cause of the initial symptoms. It is not unusual for individuals at risk of familial AD to experience considerable anxiety about the possibility of developing memory problems, which understandably accentuates as they grow close to the age at which their parent developed symptoms. The authors’ reference to the subjective memory complaints scores in the non-carriers provided one way of addressing this issue, but it would have also been interesting to know how the individuals with symptomatic pre-MCI who improved scored on the geriatric depression scale.
It is notable that all of the symptomatic participants in Acosta-Baena and colleagues’ study had objective cognitive deficits by the time they Entinostat manifested symptoms. In our experience, not all individuals who develop familial AD follow the same trajectory. Whilst objective cognitive deficits do manifest several years prior to symptoms in many patients [9], selleck chemicals others may develop memory complaints without objective impairment initially, and would conform to the conventional definition of pre-MCI.