Browsing by Subject "Nicotine"

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  • Leino, Sakari; Kohtala, Samuel; Rantamäki, Tomi; Koski, Sini K.; Rannanpää, Saara; Salminen, Outi (2018)
    BackgroundThe treatment of Parkinson's disease is often complicated by levodopa-induced dyskinesia (LID). Nicotinic acetylcholine receptor agonists can alleviate LID in animal models but may be less effective in conditions of severe dopaminergic denervation. While the mechanisms of LID remain incompletely understood, elevated corticostriatal levels of the brain-derived neurotrophic factor (BDNF) have been suggested to play a role. Here, female mice with near-total unilateral 6-hydroxydopamine-induced nigrostriatal lesions were chronically treated with levodopa, and the effects of the 7 nicotinic receptor partial agonist AZD0328 and nicotine on LID were assessed. At the end of the experiment, BDNF protein levels in the prefrontal cortex and striatum were measured.ResultsFive-day treatments with three escalating doses of AZD0328 and a 10-week treatment with nicotine failed to alleviate LID. BDNF levels in the lesioned striatum correlated positively with LID severity, but no evidence was found for a levodopa-induced elevation of corticostriatal BDNF in the lesioned hemisphere. The nicotine treatment decreased BDNF levels in the prefrontal cortex but had no effect on striatal BDNF.ConclusionsThe findings suggest that treatment of LID with nicotinic agonists may lose its effectiveness as the disease progresses, represent further evidence for a role for BDNF in LID, and expand previous knowledge on the effects of long-term nicotine treatment on BDNF.
  • Leino, Sakari; Kohtala, Samuel; Rantamäki, Tomi; Koski, Sini K; Rannanpää, Saara; Salminen, Outi (BioMed Central, 2018)
    Abstract Background The treatment of Parkinson’s disease is often complicated by levodopa-induced dyskinesia (LID). Nicotinic acetylcholine receptor agonists can alleviate LID in animal models but may be less effective in conditions of severe dopaminergic denervation. While the mechanisms of LID remain incompletely understood, elevated corticostriatal levels of the brain-derived neurotrophic factor (BDNF) have been suggested to play a role. Here, female mice with near-total unilateral 6-hydroxydopamine-induced nigrostriatal lesions were chronically treated with levodopa, and the effects of the α7 nicotinic receptor partial agonist AZD0328 and nicotine on LID were assessed. At the end of the experiment, BDNF protein levels in the prefrontal cortex and striatum were measured. Results Five-day treatments with three escalating doses of AZD0328 and a 10-week treatment with nicotine failed to alleviate LID. BDNF levels in the lesioned striatum correlated positively with LID severity, but no evidence was found for a levodopa-induced elevation of corticostriatal BDNF in the lesioned hemisphere. The nicotine treatment decreased BDNF levels in the prefrontal cortex but had no effect on striatal BDNF. Conclusions The findings suggest that treatment of LID with nicotinic agonists may lose its effectiveness as the disease progresses, represent further evidence for a role for BDNF in LID, and expand previous knowledge on the effects of long-term nicotine treatment on BDNF.
  • CHD Exome Consortium; Consortium Genetics Smoking; EPIC-CVD Consortium; Understanding Soc Sci Grp; Brazel, David M.; Jiang, Yu; Hughey, Jordan M.; Loukola, Anu; Qaiser, Beenish; Kaprio, Jaakko; Kontto, Jukka; Perola, Markus; Dunning, Alison M. (2019)
    BACKGROUND: Smoking and alcohol use have been associated with common genetic variants in multiple loci. Rare variants within these loci hold promise in the identification of biological mechanisms in substance use. Exome arrays and genotype imputation can now efficiently genotype rare nonsynonymous and loss of function variants. Such variants are expected to have deleterious functional consequences and to contribute to disease risk. METHODS: We analyzed similar to 250,000 rare variants from 16 independent studies genotyped with exome arrays and augmented this dataset with imputed data from the UK Biobank. Associations were tested for five phenotypes: cigarettes per day, pack-years, smoking initiation, age of smoking initiation, and alcoholic drinks per week. We conducted stratified heritability analyses, single-variant tests, and gene-based burden tests of nonsynonymous/loss-of-function coding variants. We performed a novel fine-mapping analysis to winnow the number of putative causal variants within associated loci. RESULTS: Meta-analytic sample sizes ranged from 152,348 to 433,216, depending on the phenotype. Rare coding variation explained 1.1% to 2.2% of phenotypic variance, reflecting 11% to 18% of the total single nucleotide polymorphism heritability of these phenotypes. We identified 171 genome-wide associated loci across all phenotypes. Fine mapping identified putative causal variants with double base-pair resolution at 24 of these loci, and between three and 10 variants for 65 loci. Twenty loci contained rare coding variants in the 95% credible intervals. CONCLUSIONS: Rare coding variation significantly contributes to the heritability of smoking and alcohol use. Fine-mapping genome-wide association study loci identifies specific variants contributing to the biological etiology of substance use behavior.
  • Koljonen, Virve; Leikola, Junnu; Tukiainen, Erkki (2020)
    Nikotiini on verisuonia voimakkaasti supistava aine. Sen tiedetään haittaavan haavan paranemista ¬verisuonikouristuksen ja vähentyneen hapensaannin kautta. Tutkimusnäyttö viittaa siihen, että nikotiinia sisältävän sähkösavukkeen käyttö heikentää haavan ¬paranemista ja kudoskielekkeiden verenkiertoa. Sähkösavukkeiden käyttäjät eivät miellä itseään tupakoijiksi, joten on tärkeää kysyä sähkösavukkeista ¬erikseen. Jo nykyisen tutkimustiedon perusteella ennen elektiivistä kirurgiaa sähkösavukkeiden käyttäjiä tulisi ¬opastaa lopettamaan samalla lailla kuin tupakoijiakin.
  • Ekroos, Heikki; Reijula, Kari (2018)
    Koko hoitoketju on saatava ylläpitämään vieroitusosaamista.
  • Kaasinen, Valtteri; Lokki, Marja-Liisa (2020)
  • Patja, Kristiina; Borodulin, Katja (2020)
    • Nikotiini ei näytä parantavan voimantuottoa, kestävyyttä eikä harjoittelusta palautumista. • Nikotiinituotteita voi pitää yleisesti urheilijan elimistön puolustusjärjestelmän kannalta haitallisina. • Nikotiinia ei ole luokiteltu dopingaineeksi (WADA), mikä kertoo siitä, ettei sen käyttö paranna urheilijan suorituskykyä. • Kilpaurheilijoilla nikotiinituotteiden käyttö perustuu uskomuksiin ja samanlaisiin kemiallisen riippuvuuden kokemuksiin kuin muillakin niistä riippuvaisilla henkilöillä.