Kognitív epidemiológia – Az intelligenciaszint prospektív összefüggése a szomatikus és pszichiátriai betegségrizikóval

Cognitive epidemiology is the science of the relationship between intelligence and health. Modern studies of cognitive epidemiology, often with samples of several hundreds of thousands of individuals, have revealed that higher premorbid intelligence is associated with a lower risk of virtually all of mental illnesses and psychiatric problems. Higher premorbid intelligence is also associated negatively with the incidence of mortality, circulatory illness, metabolic illness, poor health behavior and many diseases of lower epidemiological significance, but its relationship to respiratory illness and nonsmoking related cancers is weaker or nonexistent. Indicators of adult socioeconomic status do not mediate the association between intelligence and mental illness, but they do partially mediate the relationship with somatic illness and mortality. Studies with special designs – twin control studies, pseudo-experimental studies and molecular genetic studies using Mendelian randomization – suggest that the relationship between intelligence and health is heavily mediated by genetic factors, but somatic health may be modestly but causally improved by better social status as a consequence of higher intelligence. © 2021 Szerző(k

Epilepsy as a derailment of sleep plastic functions may cause chronic cognitive impairment - A theoretical review

We report on a peculiar way of chronic cognitive impairment associated with interictal epileptic activity during NREM sleep. We review three major groups of epilepsy: mesiotemporal epilepsy (MTLE) involving the epileptic derailment of the hippocampal declarative memory system; childhood developmental epileptic encephalopathies; and the spectrum disorders of the perisylvian communication network with the centrotemporal spike phenomenon, overarching child- and adulthood epilepsies, totaling up the majority of epilepsies in childhood. We outline high impact research-lines on the cognitive harm of epilepsy; causing specific or global cognitive decline through its interference with sleep plastic functions. We highlight the key role of interictal activity in the development of cognitive impairment and the fact that we are unarmed against this harm, antiepileptic pharmaco-therapy being ineffective against the interictal process marked by spikes and high frequency oscillations

Individual slow wave morphology is a marker of ageing

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Lateralized rhythmic acoustic stimulation during daytime NREM sleep enhances slow waves

Slow wave sleep (SWS) is characterized by the predominance of delta waves and slow oscillations, reflecting the synchronized activity of large cortical neuronal populations. Amongst other functions, SWS plays a crucial role in the restorative capacity of sleep. Rhythmic acoustic stimulation (RAS) during SWS has been shown a cost-effective method to enhance slow wave activity. Slow wave activity can be expressed in a region-specific manner as a function of previous waking activity. However, it is unclear whether slow waves can be enhanced in a region-specific manner using RAS. We investigated the effects of unilaterally presented rhythmic acoustic sound patterns on sleep electroencephalographic (EEG) oscillations. Thirty-five participants received during SWS 12-second long rhythmic bursts of pink noise (at a rate of 1 Hz) that alternated with non-stimulated, silent periods, unilaterally delivered into one of the ears of the participants. As expected, RAS enhanced delta power, especially in its low-frequency components between 0.75 and 2.25 Hz. However, increased slow oscillatory activity was apparent in both hemispheres regardless of the side of the stimulation. The most robust increases in slow oscillatory activity appeared during the first 3-4 seconds of the stimulation period. Furthermore, a short-lasting increase in theta and sigma power was evidenced immediately after the first pulse of the stimulation sequences. Our findings indicate that lateralized RAS has a strong potential to globally enhance slow waves during daytime naps. The lack of localized effects suggests that slow waves are triggered by the ascending reticular system and not directly by specific auditory pathways

Increased cortical involvement and synchronization during CAP A1 slow waves

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Sleep EEG functional connectivity varies with age and sex, but not general intelligence

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