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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F13%3A43908191%21RIV14-MSM-11120___
rdf:type
skos:Concept n20:Vysledek
dcterms:description
Cognitive deficit represents the core impairment in schizophrenia that fundamentally affects course and functional outcome of illness. Thus far, generally held views claim that conventional antipsychotics are less effective in cognitive remediation; furthermore, cognition may be worsened by the adjuvant anticholinergic medication used to alleviate from side effects. However, several earlier and recent reports indicated that a low dosage of typical antipsychotics may possess procognitive properties. Unequivocally positive effects of virtually all second-generation antipsychotics in remediation of a cognitive deficit have been shown in both individual studies and meta-analyses. The key role in cognition is played by dopamine activity in the prefrontal cortex. Dopamine action is mediated through D1 receptors, as evidenced by the improvement of cognitive performance following administration of D1 agonists. Stimulation of dopamine neurotransmission is rate-limited: low doses enhance cognition whereas higher doses may cause cognitive impairments. Dopamine activity can be also modulated indirectly, via serotonin receptor system, either with 5-HT1a agonists or 5-HT2 antagonists. Cognitive deficit represents the core impairment in schizophrenia that fundamentally affects course and functional outcome of illness. Thus far, generally held views claim that conventional antipsychotics are less effective in cognitive remediation; furthermore, cognition may be worsened by the adjuvant anticholinergic medication used to alleviate from side effects. However, several earlier and recent reports indicated that a low dosage of typical antipsychotics may possess procognitive properties. Unequivocally positive effects of virtually all second-generation antipsychotics in remediation of a cognitive deficit have been shown in both individual studies and meta-analyses. The key role in cognition is played by dopamine activity in the prefrontal cortex. Dopamine action is mediated through D1 receptors, as evidenced by the improvement of cognitive performance following administration of D1 agonists. Stimulation of dopamine neurotransmission is rate-limited: low doses enhance cognition whereas higher doses may cause cognitive impairments. Dopamine activity can be also modulated indirectly, via serotonin receptor system, either with 5-HT1a agonists or 5-HT2 antagonists.
dcterms:title
6. Pharmacological management of cognitive deficit in schizophrenia 6. Pharmacological management of cognitive deficit in schizophrenia
skos:prefLabel
6. Pharmacological management of cognitive deficit in schizophrenia 6. Pharmacological management of cognitive deficit in schizophrenia
skos:notation
RIV/00216208:11120/13:43908191!RIV14-MSM-11120___
n20:predkladatel
n21:orjk%3A11120
n3:aktivita
n7:P
n3:aktivity
P(1M0517)
n3:dodaniDat
n4:2014
n3:domaciTvurceVysledku
n17:1965247
n3:druhVysledku
n11:C
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n14:predkladatel
n3:idSjednocenehoVysledku
119930
n3:idVysledku
RIV/00216208:11120/13:43908191
n3:jazykVysledku
n10:eng
n3:klicovaSlova
glutamate; norepinephrine; dopamine; antipsychotics; cognition; schizophrenia
n3:klicoveSlovo
n5:schizophrenia n5:glutamate n5:norepinephrine n5:dopamine n5:antipsychotics n5:cognition
n3:kontrolniKodProRIV
[39F250B7BE67]
n3:mistoVydani
New York
n3:nazevZdroje
Cognitive Deficit in Mental and Neurological Disorders
n3:obor
n12:FL
n3:pocetDomacichTvurcuVysledku
1
n3:pocetStranKnihy
469
n3:pocetTvurcuVysledku
1
n3:projekt
n9:1M0517
n3:rokUplatneniVysledku
n4:2013
n3:tvurceVysledku
Mohr, Pavel
s:numberOfPages
13
n18:hasPublisher
Nova Science Publishers
n13:isbn
978-1-60741-957-0
n15:organizacniJednotka
11120