Akutna primjena nikotina ne poboljšava kognitivne funkcije

Chronic smokers often claim that smoking improves their cognitive abilities, such as concentration. However, scientific evidence to support this claim is scarce. Previous studies gave inconclusive results, and some of them had significant methodological flaws. Therefore, the aim of this study was to test whether smoking a single cigarette affects performance across several cognitive domains. It included a group of 22 occasional smokers aged 19–29 years. Attention, working memory, and visuospatial reasoning were assessed using a within-subjects design with a control setting. There were two separate testing sessions two days apart. Half the group started with experimental and the other half with control setting. In the experimental setting, the participants completed the first block of tasks, smoked one cigarette (with a nicotine yield of 0.5 mg), and then completed the second block of tasks. In the control setting, the procedure was the same, except that the participants had a glass of water instead of a cigarette. Repeated measures ANOVA showed no significant effects of cigarette smoking on either reaction time rates or accuracy on any of the three cognitive domains. These results suggest that, at least among young, occasional smokers, smoking does not affect cognition and the claims of its improvement are probably a result of some sort of cognitive bias.Kronični pušači često tvrde da im pušenje, između ostaloga, pozitivno utječe na kognitivne sposobnosti (npr. pomaže im u održavanju koncentracije). Je li doista tako još uvijek nemamo jednoznačan odgovor, budući da su prethodne studije ne samo dale nekonzistentne rezultate nego su bile i metodološki manjkave. Stoga je cilj ovoga istraživanja bio utvrditi utječe li konzumacija jedne cigarete na izvedbu zadataka u nekoliko različitih kognitivnih domena. U istraživanju je sudjelovala skupina povremenih pušača u dobi od 19 do 29 godina. Pomoću računalnog programa E-Prime prezentirani su zadaci koji mjere pažnju, radno pamćenje i obradu vidno-prostornih informacija. Korišten je prije-poslije nacrt, uz kontrolni i eksperimentalni uvjet. Sudionici su iste zadatke rješavali četiri puta: prije i poslije tretmana u kontrolnom uvjetu te prije i poslije tretmana u eksperimentalnom uvjetu. U kontrolnom uvjetu tretman se sastojao od čaše vode koju su sudionici morali popiti, a u eksperimentalnom uvjetu od pušenja jedne cigarete koja otpušta 0,5 mg nikotina. Stanka između kontrolnoga i eksperimentalnoga testiranja bila je dva dana. Redoslijed uvjeta bio je rotiran. Niti u jednom zadatku nije utvrđen značajan utjecaj pušenja ni na vrijeme reakcije ni na točnost rješavanja. Ovi su nalazi u skladu s hipotezom da su samoiskazi o pozitivnom utjecaju pušenja na kognitivnu učinkovitost posljedica neutemeljenih subjektivnih dojmova

Molecular mechanisms of brain ageing

Starenje je multifaktorijalni proces koji je pod utjecajem kumulativnih fizioloških promjena. One su rezultat stohastičnih procesa i genetskih promjena koje zajedno mijenjaju homeostazu organizma. Starenje pogađa sve organske sustave, pa tako i živčani sustav koji, zbog specifičnosti svoje stanične građe, ima dodatne mehanizme koji doprinose starenju. Kao i u periferiji, dolazi do akumulacije reaktivnih kisikovih spojeva i disfunkcije mitohondrija što dovodi do nakupljanja oštećenih staničnih komponenti i smanjivanja proizvodnje energije. To rezultira smanjenom funkcionalnošću stanica. Uz to, dolazi do mutacija i promijenjene genetičke ekspresije što dovodi do mijenjanja staničnih signalnih puteva, zbog čega dolazi do promjena u staničnoj morfologiji i funkcionalnosti. Promjene u neurotransmiterskom signaliziranju, disregulacija kalcija te promijenjena ekspresija ionskih kanala dovode do promjena u provođenju signala, smanjenoj plastičnosti sinapsa i neurona. Smanjenje neurotrofnih faktora dovodi do smanjene neurogeneze, smanjenog nicanja dendritnih nastavaka i dendrita. To dovodi do smanjenog volumena mozga. Svi ovi faktori dovode do promjena koje možemo uočiti kod osoba starije životne dobi poput smanjenja kognitivnih sposobnosti, u što ubrajamo gubitak pamćenja i smanjenje sposobnosti učenja, kao i promjene u raspoloženju i ponašanju. Sve te promjene se događaju kod normalnog starenja, ali se puno jači, slični simptomi javljaju kod osoba oboljelih od neurodegenerativnih bolesti. No, životnim stilom i promjenama u prehrani može se utjecati da se ublaže simptomi neuralnog starenja.Aging is a multifactor process induced by cumulative physiological changes that are a result of stochastic processes and differentiation in genetic expression which result in an altered homeostasis. Therefore, it affects all organ systems, as well as the neurological system which has other, specific, age-related mechanisms that are unique to the aging brain. As well as in the periphery, there is a rise in reactive oxygen species which leads to mitochondrial dysfunction. Also, damaged cellular compartments accumulate and energy production is decreased which results in decreased cellular functionality. Furthermore, mutations and altered genetic expression results in altered signalling pathways which consequentially ends up in different cellular morphology and functionality. Changes in neurotransmitter signalling, calcium dysgulation and expression of ion channels leads to signal transmission disruptions and decreased synaptic plasticity. Furthermore, decrease in neurotrophic factors results in decreased neurogenesis, smaller amount of dendrites and dendritic projections which affects the brain volume. All these factors are a direct cause of the age-related physical changes such as decreased cognitive abilities, alternations in mood and behaviour. These symptoms are observed in normal aging as well as in neurodegenerative diseases, but in a more fatal form. Nonetheless, with our lifestyle and dietary restriction we can influence the onset and the magnitude of the symptoms of neural aging

Exploring the cognitive schemas as individual or group structures

V prispevku je predstavljenih nekaj značilnosti teorije kognitivnih shem. Ukvarjali smo se z vprašanjem, na kateri ravni naj se raziskujejo kognitivne sheme: na individualni-, nadindividualni-, ali celo na ravni večjih socialnih sistemov, in sicer glede na značilnosti socialne kognicije ter glede na naravo kognitivnih shem. V zadnjem obdobju se raziskovalci kognitivnih shem osredotočajo na interakcijo med motivacijskimi, kognitivnimi in drugimi osebnimi ter situacijskimi spremenljivkami in njihovim vplivom na vedenje. Kognitivne sheme so razumljene kot rezultat medsebojnega prepleta osebnih, okoljskih in situacijskih spremenljivk. Odgovor na zastavljeno vprašanje pa je odvisen tudi od paradigme, znotraj katere raziskovalec raziskuje in od raziskovalnega problema.The present paper describes some features of the theory of cognitive schemas. The discussion focuses on the issue of appropriate level to explore the cognitive schemas: the individual-, above individual- or the level of larger social systems, depending on the characteristics of social cognition and the nature of cognitive schemas. Currently researchers of cognitive schemas focus on the interaction between motivational, cognitive and other personal and situational variables and on their influence on behavior. Cognitive schemas are seen as the result of mutual interplay between personal, environmental and situational variables. The answer to the appropriate level of exploration question is found to depend on the paradigm within which the individual researchers work and also on the nature of the research problem

Treatment Approach to Alzheimer’s Disease

Alzheimerova bolest (AB) je neurodegenerativna bolest mozga i najčešći oblik demencije. Radi se o sindromu sa progresivnim gubitkom kognitivnih funkcija popraćenom ponašajnim i psihičkim simptomima. Nakupljeni β-amiloid i neurofibrilarni snopići implicirani su u nastanku funkcionalnih i neurodegenerativnih promjena koje završavaju smrću stanice. Etiološko liječenje zasad ne postoji. Aktualne mogućnosti farmakološkog liječenja sastoje se od dviju skupina lijekova: inhibitori kolinesteraze (donepezil, galantamin, rivastigmin) i antagonisti NDMA receptora, koji su se pokazali učinkoviti u poboljšanju kognitivnih funkcija, pojedini i s utjecajem na bihevioralne simptome. Ni jedan od ovih lijekova ne mijenja tijek i ishod bolesti. Istražuju se nove supstancije koje ciljaju na metabolizam amiloida i tau proteina. Od neuromodulacijskih metoda najviše se istražuju rTMS i tDCS, koji su pokazali pozitivne učinke na kognitivne funkcije. Kognitivna stimulacija također ima pozitivne rezultate pa se sve više istražuju učinci neuromodulatorskih metoda liječenja kombiniranih s kognitivnim vježbama, što je u praksi moguće putem sustava NeuroAD™Alzheimer’s disease (AD) is a neurodegenerative brain disorder and the most common type of dementia. AD is a syndrome leading to progressive loss of cognitive functions, often followed by behavioural and psychological symptoms. Amyloid plaques and neurofibrillary tangles are implicated in functional and neurodegenerative changes leading to neuronal death. A curative treatment does not exist. Pharmacological treatments include cholinesterase inhibitors (donepezil, galantamine, rivastigmine) and NDMA receptor antagonists, which have been shown to improve cognitive functions and some of them may also have positive effects on behavioural symptoms. None of these drugs effect the course and outcome of the disease. New drugs that can interfere with β-amyloid and tau protein metabolism are being researched. Neuromodulator methods of treatment such as TMS and tDCS are being researched and have shown positive effects on cognitive functions. Cognitive stimulation has also shown positive effects so it is not surprising that more research is being aimed at studying the combined effects of neuromodulator treatment and cognitive stimulation, which is in practice possible using the NeuroAD™ system