Sleep-dependent memory consolidation and accelerated forgetting.

Autor: Atherton KE; Department of Experimental Psychology, University of Oxford, Oxford, UK; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Electronic address: kat.atherton@gmail.com., Nobre AC; Department of Experimental Psychology, University of Oxford, Oxford, UK; Oxford Centre for Human Brain Activity, University of Oxford, Oxford, UK., Zeman AZ; Cognitive and Behavioural Neurology Research Group, University of Exeter Medical School, UK., Butler CR; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Jazyk: angličtina
Zdroj: Cortex; a journal devoted to the study of the nervous system and behavior [Cortex] 2014 May; Vol. 54, pp. 92-105. Date of Electronic Publication: 2014 Feb 21.
DOI: 10.1016/j.cortex.2014.02.009
Abstrakt: Accelerated long-term forgetting (ALF) is a form of memory impairment in which learning and initial retention of information appear normal but subsequent forgetting is excessively rapid. ALF is most commonly associated with epilepsy and, in particular, a form of late-onset epilepsy called transient epileptic amnesia (TEA). ALF provides a novel opportunity to investigate post-encoding memory processes, such as consolidation. Sleep is implicated in the consolidation of memory in healthy people and a deficit in sleep-dependent memory consolidation has been proposed as an explanation for ALF. If this proposal were correct, then sleep would not benefit memory retention in people with ALF as much as in healthy people, and ALF might only be apparent when the retention interval contains sleep. To test this theory, we compared performance on a sleep-sensitive memory task over a night of sleep and a day of wakefulness. We found, contrary to the hypothesis, that sleep benefits memory retention in TEA patients with ALF and that this benefit is no smaller in magnitude than that seen in healthy controls. Indeed, the patients performed significantly more poorly than the controls only in the wake condition and not the sleep condition. Patients were matched to controls on learning rate, initial retention, and the effect of time of day on cognitive performance. These results indicate that ALF is not caused by a disruption of sleep-dependent memory consolidation. Instead, ALF may be due to an encoding abnormality that goes undetected on behavioural assessments of learning, or by a deficit in memory consolidation processes that are not sleep-dependent.
(Copyright © 2014 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Databáze: MEDLINE
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