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Björn Rasch

Publications and source records attributed to Björn Rasch.

3 recordsLinked to original sources

A 3-day estrogen treatment improves prefrontal cortex-dependent cognitive function in postmenopausal women.

Estrogen secretion in young women follows a cyclic pattern characterized by a pronounced surge in estrogen around ovulation. The way in which this estrogen peak affects cognitive functioning is unclear. Short-term estrogen treatment for a few days mimicking normal pre-menopausal estrogen dynamics substantially enhanced cognitive functions in ovariectomized animals. Here, we provide evidence that inducing a single estrogen peak in postmenopausal women improves their cognitive abilities. Healthy women (51-64 yrs, n=14) received either 100 microg estrogen transdermally for 3 days or placebo in a double-blind within-subject design. The treatment caused a temporary rise in serum estrogen levels roughly comparable to the mid-cyclic changes in estrogen in young women. At the end of the treatment, the women completed two types of tests involving primarily hippocampus-dependent functions of memory retention or prefrontal cortex-dependent functions. Results revealed a clear beneficial effect of estrogen on tasks mainly involving the prefrontal cortex: performance on a digit-ordering task (p<0.05) and on a task requiring short-term memory of event sequences in an unfamiliar story (p<0.01) were improved, and susceptibility to interference in the Stroop test (p<0.05) was diminished after estrogen. On the other hand, estrogen did not affect hippocampus-dependent retention of a story, with delayed recall tested after 30 min or 1 week, although immediate recall was improved by estrogen. We conclude that in postmenopausal women, a transient increase in plasma estrogen concentration acutely improves prefrontal cortex-dependent cognitive functions, whereas hippocampus-dependent memory retention is less affected. Our results encourage future studies to investigate whether repeated induction of short-lasting estrogen peaks could enhance cognitive efficacy of hormonal replacement therapy.

Administration, Cutaneous↗

Brief sleep after learning keeps emotional memories alive for years.

BACKGROUND: Sleep after learning supports memory consolidation. However, long-lasting memory effects of sleep have not yet been investigated. Postlearning sleep may be particularly involved in the long-term retention of emotional memories and could thereby contribute to the development of posttraumatic stress disorder (PTSD), a disease thought to result from overconsolidation of traumatic memories. METHODS: Subjects (healthy men) who had learned neutral and emotional texts immediately before sleeping or remaining awake for the subsequent 3 hours were recontacted after 4 years for long-term memory assessment (forced-choice recognition test). RESULTS: Sleep following learning compared with wakefulness enhanced memory for emotional texts after 4 years (p = .001). No such enhancement was observed for neutral texts (p = .571). CONCLUSIONS: Brief periods of sleep immediately following learning cause preservation of emotional memories over several years. Sleep deprivation in the immediate aftermath of traumatic events could be a promising therapeutic measure to prevent PTSD.

Chi-Square Distribution↗

Sleep to remember.

Recently, compelling evidence has accumulated that links sleep to learning and memory. Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory. Consolidation is an active process that is presumed to rely on the covert reactivation and reorganization of newly encoded representations. Hippocampus-dependent memories benefit primarily from slow-wave sleep (SWS), whereas memories not depending on the hippocampus show greater gains over periods containing high amounts of rapid eye movement sleep. One way sleep does this is by establishing different patterns of neurotransmitters and neurohormone secretion between sleep stages. Another central role for consolidating memories is played by the slow oscillation, that is, the oscillating field potential change dominating SWS. The emergence of slow oscillations in neocortical networks depends on the prior use of these networks for encoding of information. Via efferent pathways, they synchronize the occurrence of sharp wave ripples accompanying memory reactivations in the hippocampus with thalamocortical spindle activity. Thus, hippocampal memories are fed back into neocortical networks at a time when these networks are depolarized and, because of concurrent spindle activity, can most sensitively react to these inputs with plastic changes underlying the formation of long-term memory representations.

Animals↗