الفهرس Only 14 pages are availabe for public view
 |  | from | 188 |  |  |
| | | from | 188 | | |
Abstract
Sleep may be divided into two phases , REM and NREM sleep . The survey of neuronal and neurotransmitter - related brainstem mechanisms of REM includes monoamines ( noradrenaline and serotonin ) as REM – off neurons and acetylcholine as REM – on neurons . A new emphasis on GABAergic mechanisms with significant increase in REM sleep compared with wakefulness while SWS did not significantly differ from wakefulness . orexin could be this factor (or one of the factors) exciting the REM - off neurons, consistent with its effects on LC and DRN neurons . The effect of the NREM sleep is on the basal forebrain and adenosine as a mediator of homeostatic control . Control is through basal forebrain extracellular adenosine accumulation during wakefulness and inhibition of wakefulness - active neurons. Over longer periods of sleep loss , there is a second mechanism of homeostatic control through transcriptional modification . Adenosine acting at the A1 receptor produces an up – regulation of A1 receptors, which increases inhibition for a given level of adenosine , effectively increasing the gain of the sleep homeostat.
The most widely accepted taxonomy divides human memories first into declarative and non – declarative , based on their accessibility to conscious recall. Declarative memory refers to the retention of facts ( semantic ) and events ( episodic ) , and is neuroanatomically defined by its crucial dependence on hippocampal function. Procedural memory represents the type of nondeclarative memory that has been most extensively studied in conjunction with sleep. Procedural memory refers to memories for perceptual and motor skills with the latter essentially relying on cortico-striatal and cortico-cerebellar loops. Encoding and retrieval of memories can be explicit or implicit ( i.e. with or without awareness) although both processes normally occur in parallel . Encoding and retrieval are thought to be always explicit for declarative memories, but both modes are possible for procedural memories.
The term ‘‘memory consolidation’’ refers to a poorly defined set of processes which take an initial, unstable memory representation and convert it into a form that is both more stable and more effective. The concept of ‘‘ memory reconsolidation ’’ describe yet another aspect of post-encoding memory modification.
Explicit knowledge improves only across the night, while implicit knowledge improves across either wake or sleep . Most procedural memories show sleep - dependent enhancements duing REM sleep while declarative memories show enhancement duing early night rich in SWS sleep.
If sleep is to be considered a critical mediator of memory consolidation , then evidence of sleep - dependent plasticity would greatly strengthen this claim.
Neuroimaging , electrophysiological , cellular and molecular studies have provided a wealth of converging evidence that sleep - dependent mechanisms of neural plasticity lead to the consolidation of learning and memory . Significant numbers of genes also appear to be up - regulated specifically in brain tissue during posttraining sleep.
Aging process affects some components of memory more than others . Studies have consistently shown that secondary memory exemplified by the ability to learn information and recall it after a time delay is most strongly affected by age . studies suggest that older adults retain information at rates only slightly below that of younger adults.
Age - related changes in the amount and pattern of the various stages of sleep and wakefulness are well described. Elderly people spend more time in bed and less time asleep and are more easily aroused from sleep than are young people. The most striking changes include a reduction in slow – wave sleep ( particularly stage 4 sleep ) , increased nighttime wakefulness , and increased fragmentation of sleep by periods of wakefulness.
Dementia denotes a deterioration of intellectual, or cognitive function , with little or no disturbance of consciousness or perception.
Clinical profiles of dementia include: Alzheimer’s disease , Vascular dementia , Lewy body disease, Frontotemporal dementia, Normal pressure hydrocephlus and Prion disease.
Sleep disturbances in dementia are common and the causes of sleep disturbances in patients with dementia is thought to be multifactorial and include components specific to dementia , circadian rhythm disturbance, coexisting psychiatric conditions, medication use , sleep - disorderd breathing.
Cholinergic deficit contributes to several of the most prominent neuropsychiatric manifestations of dementia . Noradrenaline , serotonin and dopamine contribute to other BPSD in dementia but to a lesser extent than acetylcholine.
Treatment of sleep disturbances in dementia include behavioral techniques and pharmacological treatment.
Sleep deprivation produce an allostatic over load with deleterious effect on cognitive function . Several neuroimaging studies include PET and fMRI show reduced performance on different cognitive tasks following sleep deprivation, this is the immediate consequences of sleep deprivation . Also Sleep deprivation alter the slow processes leading to memory consolidation.
RBD may not simply represent an interesting parasomnia but rather reflects dysfunction in REM sleep control that has relevance for understanding certain neurodegenerative disorders. Neurodegenerative disorders most commonly associated with RBD are PD,DLB, and MSA.
REM density of the 1st REM period, total REM density, duration of the 1st REM period and REM sleep percentage were significantly lower in patients with dementia . REM latency was significantly longer in dementia. no significant differences between the groups were found regarding slow wave sleep.
Anticholinesterase compounds increases REM sleep , reduces EEG slow frequencies while increasing waking alpha rhythm, and tends to improve cognitive functions.