BACKGROUND: From 2012 to 2013, there was a mass methanol poisoning outbreak in the Czech Republic. Methanol metabolites can cause specific lesions in the basal ganglia, subcortical white matter, and optic nerve. However, long-term sequelae of methanol poisoning on cognitive functioning have not yet been explored. The current study aimed to delineate the cognitive changes observed in methanol poisoning survivors in the seven years since 2012. METHODS: We conducted longitudinal research with repeated measurements in 2013, 2015, 2017 and 2019 to evaluate the development of cognitive changes after acute methanol poisoning. A complex neuropsychological battery consisted of tests of global cognitive performance, auditory and visual attention, executive functioning, learning and memory, working memory and language. Motor performance measures and depression scale were also included. RESULTS: Repeated measures ANOVA of four measurements with post-hoc tests showed a significant decline in the Mini-Mental State Examination (p = 0.007); however, other parameters were not significantly decreasing. In comparison to normative values, the z-scores for each test measure, in the memory domain, in particular, ranged from 43 to 60 % of participants below 1.5 SD. Mild to severe depression levels from the onset of poisoning improved during the seven years, returning to normal in up to 27 % of participants. CONCLUSION: In the longitudinal perspective, methanol poisoning survivors manifest progressive global cognitive decline and overall persistent below-average cognitive performance with some improvements in the frequency of depressive symptoms.
- MeSH
- časové faktory MeSH
- deprese chemicky indukované diagnóza epidemiologie psychologie MeSH
- dospělí MeSH
- epizodická paměť * MeSH
- kognice účinky léků MeSH
- kognitivní dysfunkce chemicky indukované diagnóza epidemiologie psychologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- longitudinální studie MeSH
- methanol otrava MeSH
- mladý dospělý MeSH
- neuropsychologické testy MeSH
- neurotoxické syndromy diagnóza epidemiologie psychologie MeSH
- poruchy paměti chemicky indukované diagnóza epidemiologie psychologie MeSH
- prevalence MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika MeSH
Prenatal exposure to caffeine can cause developmental problems. This study determined chronic influence of prenatal caffeine at relatively higher doses on cognitive functions in the rat offspring. Pregnant Sprague-Dawley rats (4-month-old) were exposed to caffeine (20 mg/kg, twice a day) for whole pregnancy from gestational day 4. Fetal and offspring body and brain weight was measured. Learning and memory were tested in adult offspring with Morris water maze. Learning and memory-related receptors were measured. The exposure to prenatal caffeine not only caused fetal growth restriction, but also showed long-term effects on learning and memory in the offspring. The caffeine offspring exhibited longer escape latency and path length in navigation testing. The number of passing the target was significantly reduced in those offspring. The expression of adenosine A(1) and A(2A) receptors, nuclear PKA C(alpha), C(beta) subunits, and pCREB were significantly increased in the fetal and neonatal brain, and suppressed in the hippocampus of the adult offspring. The expression of BDNF and TrkB were reduced regardless of various ages. The results suggest that intrauterine programming dysfunction of adenosine receptors and the down-stream of cAMP/PKA/pCREB system may play an important role in prenatal caffeine induced cognition disorders in the adult offspring.
- MeSH
- bludiště - učení účinky léků fyziologie MeSH
- kofein toxicita MeSH
- krysa rodu rattus MeSH
- mozkový neurotrofický faktor metabolismus MeSH
- paměť účinky léků fyziologie MeSH
- poruchy paměti chemicky indukované diagnóza metabolismus MeSH
- potkani Sprague-Dawley MeSH
- protein vázající element responzivní pro cyklický AMP metabolismus MeSH
- proteinkinasy závislé na cyklickém AMP metabolismus MeSH
- purinergní receptory P1 metabolismus MeSH
- signální transdukce účinky léků fyziologie MeSH
- těhotenství MeSH
- zpožděný efekt prenatální expozice chemicky indukované diagnóza metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
The adipokinetic and red pigment-concentrating hormone (AKH/RPCH) family of peptides controls fat, carbohydrate, and protein metabolism in insects. In our previous study, we showed that AKH possesses antidepressant, anxiolytic, and analgesic effects, causes hyperlocomotion, and exerts neuroprotective effects and increased brain neurotrophic factors in mice. The aim of this study was to investigate the effects of Anax imperator AKH (Ani-AKH), Libellula auripennis AKH (Lia-AKH), and Phormia-Terra hypertrehalosemic hormone (Pht-HrTH) on MK-801-induced memory deterioration in the active allothetic place avoidance test (AAPA) and MK-801-induced sensorimotor gating deficit in the prepulse inhibition test (PPI). In the AAPA task, Long-Evans rats were treated with Ani-AKH (2 mg/kg), Lia-AKH (2 mg/kg), Pht-HrTH (2 mg/kg), MK-801 (0.15 mg/kg), and the combination of MK-801 with the hormones subchronically. In the prepulse inhibition test, Wistar albino rats were treated with Ani-AKH (1 mg/kg), Lia-AKH (1 mg/kg), Pht-HrTH (1 mg/kg), MK-801 (0.1 mg/kg), or the combination of MK-801 with hormones acutely before the test. In our study, Ani-AKH (2 mg/kg), Lia-AKH (2 mg/kg), and Pht-HrTH (2 mg/kg) reversed MK-801 (0.15 mg/kg)-induced cognitive memory impairment effects in the AAPA task. Lia-AKH (1 mg/kg) significantly potentiated the MK-801-induced PPI disruption, while Ani-AKH (1 mg/kg) partially potentiated the impairment caused by MK-801, and Pht-HrTH did not modify the effect of MK-801. In conclusion, AKH had no effect in sensorimotor gating deficits in the PPI test in schizophrenia model while AKH improved memory in the schizophrenia model of MK-801.
- MeSH
- anxiolytika farmakologie MeSH
- dizocilpinmaleát farmakologie MeSH
- hmyzí hormony farmakologie MeSH
- krysa rodu rattus MeSH
- kyselina pyrrolidonkarboxylová analogy a deriváty farmakologie MeSH
- modely nemocí na zvířatech MeSH
- neuropeptidy farmakologie MeSH
- neuroprotektivní látky MeSH
- oligopeptidy farmakologie MeSH
- paměť účinky léků MeSH
- peptidy farmakologie MeSH
- poruchy paměti chemicky indukované farmakoterapie MeSH
- potkani Long-Evans MeSH
- potkani Wistar MeSH
- schizofrenie chemicky indukované farmakoterapie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13 years), 3-8 months after methanol poisoning, and 57 control subjects (CS; age 49 ± 13 years) were administered a neuropsychological battery. Forty-six patients were followed in 2 years' perspective. Patients additionally underwent 1.5T magnetic resonance imaging (MRI). Three biochemical and toxicological metabolic markers and a questionnaire regarding alcohol abuse facilitated the classification of 24 patients with methanol poisoning without alcohol abuse (METHna) and 22 patients with methanol poisoning and alcohol abuse (METHa). All groups were compared to a control group of similar size, and matched for age, education, premorbid intelligence level, global cognitive performance, and level of depressive symptoms. Using hierarchical multiple regression we found significant differences between METH and CS, especially in executive and memory domains. METHa showed a similar pattern of cognitive impairment with generally more severe executive dysfunction. Moreover, all METH patients with extensive involvement on brain MRI (lesions in ≥2 anatomical regions) had a more severe cognitive impairment. From a longitudinal perspective, we did not find any changes in their cognitive functioning after 2 years' follow-up. Our findings suggest that methanol poisoning is associated with executive dysfunction and explicit memory impairment, supposedly due to basal ganglia dysfunction and disruption of frontostriatal circuitry proportional to the number of brain lesions, and that these changes are persistent after 2 years' follow-up.
- MeSH
- časové faktory MeSH
- dospělí MeSH
- exekutivní funkce * MeSH
- kognitivní poruchy chemicky indukované diagnostické zobrazování psychologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- longitudinální studie MeSH
- methanol otrava MeSH
- následné studie MeSH
- neuropsychologické testy MeSH
- poruchy paměti chemicky indukované diagnostické zobrazování psychologie MeSH
- průřezové studie MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
OBJECTIVE: Lithium has been long used in psychiatry as an adjuvant treatment for bipolar disorder. Chronic lithium intoxication is very rare. DESIGN: We present the case of a 72-year-old female, treated with lithium for more than 10 years for bipolar disorder, who was admitted for gait impairment with weakness of limbs, myoclonus, speech impairment and memory disturbances. RESULTS: Diagnosis of lithium intoxication was based on clinical picture and determination of serum lithium levels. EEG showed severe encephalopathy with triphasic wave complexes. Sensory and motor axonal neuropathy was observed by EMG. Discontinuation of the drug leads to clinical improvement, although not to a fully neurological recovery. CONCLUSION: Lithium is still very effective drug, but requires regular monitoring of serum levels to prevent overdose and symptoms of intoxication. Neurophysiological methods, including EEG and EMG, are strongly recommended to determine the level of peripheral and/or central nervous system impairment.
- MeSH
- antimanika škodlivé účinky krev terapeutické užití MeSH
- bipolární porucha krev farmakoterapie patofyziologie MeSH
- elektroencefalografie MeSH
- lidé MeSH
- lithiumkarbonát škodlivé účinky krev terapeutické užití MeSH
- myoklonus krev chemicky indukované patofyziologie MeSH
- nemoci mozku krev chemicky indukované patofyziologie MeSH
- poruchy paměti krev chemicky indukované patofyziologie MeSH
- senioři MeSH
- Check Tag
- lidé MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- kazuistiky MeSH
Alzheimer's disease (AD) is a primary cause of dementia in the middle-aged and elderly worldwide. Animal models for AD are widely used to study the disease mechanisms as well as to test potential therapeutic agents for disease modification. Among the non-genetically manipulated neuroinflammation models for AD, lipopolysaccharide (LPS)-induced animal model is commonly used. This review paper aims to discuss the possible factors that influence rats' response following LPS injection. Factors such as dose of LPS, route of administration, nature and duration of exposure as well as age and gender of animal used should be taken into account when designing a study using LPS-induced memory impairment as model for AD.
- MeSH
- Alzheimerova nemoc chemicky indukované metabolismus patologie MeSH
- krysa rodu rattus MeSH
- lidé MeSH
- lipopolysacharidy toxicita MeSH
- mediátory zánětu metabolismus MeSH
- modely nemocí na zvířatech * MeSH
- poruchy paměti chemicky indukované metabolismus patologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- MeSH
- lidé středního věku MeSH
- lidé MeSH
- parestezie chemicky indukované MeSH
- poruchy paměti chemicky indukované MeSH
- postmenopauzální osteoporóza * farmakoterapie MeSH
- thiofeny * aplikace a dávkování škodlivé účinky MeSH
- úzkostné poruchy chemicky indukované MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- kazuistiky MeSH
The military incapacitating agent BZ (3-quinuclidinyl benzilate) is an anticholinergic compound that acts at both, the peripheral and central nervous system. Effects of the agent were discovered during the Cold War and BZ became one of the most potent anticholinergic psychomimetics, characterized by low effective doses causing long-term incapacitation. History, characteristics and potential use of BZ in behavioral research are discussed throughout this review.
- MeSH
- antagonisté muskarinových receptorů toxicita MeSH
- chemické bojové látky toxicita MeSH
- chinuklidinylbenzilát farmakologie toxicita MeSH
- chování zvířat účinky léků MeSH
- krysa rodu rattus MeSH
- poruchy paměti chemicky indukované MeSH
- poruchy učení chemicky indukované MeSH
- potkani Wistar MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
- přehledy MeSH
- MeSH
- antagonismus léků MeSH
- antagonisté muskarinových receptorů aplikace a dávkování kontraindikace škodlivé účinky MeSH
- diferenciální diagnóza MeSH
- hodnocení rizik MeSH
- inkontinence moči diagnóza farmakoterapie MeSH
- kongresy jako téma MeSH
- lékové předpisy MeSH
- lidé MeSH
- polypharmacy MeSH
- poruchy paměti etiologie chemicky indukované MeSH
- senioři MeSH
- Check Tag
- lidé MeSH
- senioři MeSH
- Publikační typ
- novinové články MeSH
