scholarly journals Tobacco addiction in individuals with schizophrenia: A study in rats

2021 ◽  
Author(s):  
◽  
Uta Waterhouse
Keyword(s):  
Selective Attention ◽  
Prenatal Exposure ◽  
Cognitive Deficits ◽  
Cognitive Impairments ◽  
The Self ◽  
Self Medication ◽  
Tobacco Addiction ◽  
Schizophrenic Patients ◽  
Common Substrate ◽  
The Common

<p>Schizophrenia as with most mental disorders develops due to an interaction of multiple genetic and environmental factors. Prenatal exposure to a maternal immuneactivation (MIA) is an environmental risk factor that can predispose offspring to develop schizophrenia later in life. The neurodevelopmental theory suggests that an immunechallenge during gestation can lead to long-lasting impairments such as in learning, memory,attention, or language (Brown & Patterson, 2012). Based on findings in human studies,prenatal exposure to a MIA has been utilized in preclinical research. Thus, the first aim of this study was to establish an animal model that generates subjects with schizophrenia-like cognitive impairments. To this end, a bacterial endotoxin, lipopolysaccharide (LPS) was used, which like most infectious agents, cannot cross the blood-placenta-barrier, yet reliably mimics an infection and initiates a MIA. Pregnant rats were subcutaneously (sc) injected with LPS (0.5 mg/kg) at one of three important neurodevelopmental time periods, gestation days (GD) 10/11, 15/16 or 18/19 (Fortier, Luheshi, & Boksa, 2007; Graciarena, Depino, & Pitossi, 2010). As individuals with schizophrenia commonly show deficits in multiple domains, three assessment paradigms were used to examine sensory and cognitive abilities in early and late adulthood. Tasks included prepulse inhibition to assess sensorimotor gating, latent inhibition to measure selective attention, and delayed non-matching to sample to evaluate working memory (WM).  Several theories have been suggested to explain high smoking incidence in schizophrenic patients (75-90%) compared to the general population (23%). The self-medication theory suggests high smoking rates amongst patients because nicotine, the primary addictive constituent in tobacco smoke, ameliorates some of the symptoms of the disorder such as cognitive deficits (D'Souza & Markou, 2012). Thus, the second aim of this study was to determine whether repeated experimenter and self-administered nicotine ameliorates or reduces schizophrenia-like cognitive deficits. Finally, the third aim was to investigate the common substrate theory, which suggests that shared underlying biological pathways may lead to increased susceptibility for an individual to develop both schizophrenia and tobacco addiction (Chambers, Krystal, & Self, 2001).  In conclusion, the findings of this study were coherently consistent and revealed that firstly, prenatal exposure to MIA early during foetal development led to long-lasting deficits in cognitive domains such as selective attention and WM. Secondly, supporting the self-medication theory, nicotine reversed MIA-induced cognitive impairments independent of the administration paradigm. Thirdly, increased responding rates for nicotine during self-administration acquisition in animals prenatally exposed to MIA were observed, yet there was no effect of prenatal treatment in dose response or progressive ratio testing. Thus, these findings only offer weak support for the common substrate theory.  Importantly, the findings of this study revealed that animals can be repeatedly assessed in these paradigms to examine the therapeutic efficacy of drugs and other treatments. This is of particular importance considering the lack of effective pharmacological treatments for cognitive deficits in schizophrenic patients.</p>

scholarly journals Tobacco addiction in individuals with schizophrenia: A study in rats

2021 ◽  
Author(s):  
◽  
Uta Waterhouse
Keyword(s):  
Selective Attention ◽  
Prenatal Exposure ◽  
Cognitive Deficits ◽  
Cognitive Impairments ◽  
The Self ◽  
Self Medication ◽  
Tobacco Addiction ◽  
Schizophrenic Patients ◽  
Common Substrate ◽  
The Common

<p>Schizophrenia as with most mental disorders develops due to an interaction of multiple genetic and environmental factors. Prenatal exposure to a maternal immuneactivation (MIA) is an environmental risk factor that can predispose offspring to develop schizophrenia later in life. The neurodevelopmental theory suggests that an immunechallenge during gestation can lead to long-lasting impairments such as in learning, memory,attention, or language (Brown & Patterson, 2012). Based on findings in human studies,prenatal exposure to a MIA has been utilized in preclinical research. Thus, the first aim of this study was to establish an animal model that generates subjects with schizophrenia-like cognitive impairments. To this end, a bacterial endotoxin, lipopolysaccharide (LPS) was used, which like most infectious agents, cannot cross the blood-placenta-barrier, yet reliably mimics an infection and initiates a MIA. Pregnant rats were subcutaneously (sc) injected with LPS (0.5 mg/kg) at one of three important neurodevelopmental time periods, gestation days (GD) 10/11, 15/16 or 18/19 (Fortier, Luheshi, & Boksa, 2007; Graciarena, Depino, & Pitossi, 2010). As individuals with schizophrenia commonly show deficits in multiple domains, three assessment paradigms were used to examine sensory and cognitive abilities in early and late adulthood. Tasks included prepulse inhibition to assess sensorimotor gating, latent inhibition to measure selective attention, and delayed non-matching to sample to evaluate working memory (WM).  Several theories have been suggested to explain high smoking incidence in schizophrenic patients (75-90%) compared to the general population (23%). The self-medication theory suggests high smoking rates amongst patients because nicotine, the primary addictive constituent in tobacco smoke, ameliorates some of the symptoms of the disorder such as cognitive deficits (D'Souza & Markou, 2012). Thus, the second aim of this study was to determine whether repeated experimenter and self-administered nicotine ameliorates or reduces schizophrenia-like cognitive deficits. Finally, the third aim was to investigate the common substrate theory, which suggests that shared underlying biological pathways may lead to increased susceptibility for an individual to develop both schizophrenia and tobacco addiction (Chambers, Krystal, & Self, 2001).  In conclusion, the findings of this study were coherently consistent and revealed that firstly, prenatal exposure to MIA early during foetal development led to long-lasting deficits in cognitive domains such as selective attention and WM. Secondly, supporting the self-medication theory, nicotine reversed MIA-induced cognitive impairments independent of the administration paradigm. Thirdly, increased responding rates for nicotine during self-administration acquisition in animals prenatally exposed to MIA were observed, yet there was no effect of prenatal treatment in dose response or progressive ratio testing. Thus, these findings only offer weak support for the common substrate theory.  Importantly, the findings of this study revealed that animals can be repeatedly assessed in these paradigms to examine the therapeutic efficacy of drugs and other treatments. This is of particular importance considering the lack of effective pharmacological treatments for cognitive deficits in schizophrenic patients.</p>

P.4.19 Nicotine consumption and cognitive deficits in first episode psychosis; the self medication hypothesis

2009 ◽  
Vol 19 ◽  
pp. S95-S96
Author(s):  
A. Zabala ◽  
R. Segarra ◽  
E. Elizagarate ◽  
J. Ezcurra ◽  
A. González Pinto ◽  
...  
Keyword(s):  
Cognitive Deficits ◽  
First Episode Psychosis ◽  
The Self ◽  
First Episode ◽  
Self Medication ◽  
Episode Psychosis ◽  
Nicotine Consumption

scholarly journals Genetic factors influencing a neurobiological substrate for psychiatric disorders

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Till F. M. Andlauer ◽  
Thomas W. Mühleisen ◽  
Felix Hoffstaedter ◽  
Alexander Teumer ◽  
Katharina Wittfeld ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Genetic Risk ◽  
Meta Analysis ◽  
Anterior Cingulate ◽  
Psychiatric Disease ◽  
Salience Network ◽  
Genome Wide Association Studies ◽  
Genome Wide ◽  
Common Substrate ◽  
The Common

AbstractA retrospective meta-analysis of magnetic resonance imaging voxel-based morphometry studies proposed that reduced gray matter volumes in the dorsal anterior cingulate and the left and right anterior insular cortex—areas that constitute hub nodes of the salience network—represent a common substrate for major psychiatric disorders. Here, we investigated the hypothesis that the common substrate serves as an intermediate phenotype to detect genetic risk variants relevant for psychiatric disease. To this end, after a data reduction step, we conducted genome-wide association studies of a combined common substrate measure in four population-based cohorts (n = 2271), followed by meta-analysis and replication in a fifth cohort (n = 865). After correction for covariates, the heritability of the common substrate was estimated at 0.50 (standard error 0.18). The top single-nucleotide polymorphism (SNP) rs17076061 was associated with the common substrate at genome-wide significance and replicated, explaining 1.2% of the common substrate variance. This SNP mapped to a locus on chromosome 5q35.2 harboring genes involved in neuronal development and regeneration. In follow-up analyses, rs17076061 was not robustly associated with psychiatric disease, and no overlap was found between the broader genetic architecture of the common substrate and genetic risk for major depressive disorder, bipolar disorder, or schizophrenia. In conclusion, our study identified that common genetic variation indeed influences the common substrate, but that these variants do not directly translate to increased disease risk. Future studies should investigate gene-by-environment interactions and employ functional imaging to understand how salience network structure translates to psychiatric disorder risk.

scholarly journals Zebrafish Models to Study New Pathways in Tauopathies

2021 ◽  
Vol 22 (9) ◽  
pp. 4626
Author(s):  
Clément Barbereau ◽  
Nicolas Cubedo ◽  
Tangui Maurice ◽  
Mireille Rossel
Keyword(s):  
Cognitive Deficits ◽  
Tau Protein ◽  
Common Point ◽  
Transgenic Models ◽  
Synaptic Loss ◽  
Wide Range ◽  
Transgenic Lines ◽  
Functional Consequences ◽  
The Common

Tauopathies represent a vast family of neurodegenerative diseases, the most well-known of which is Alzheimer’s disease. The symptoms observed in patients include cognitive deficits and locomotor problems and can lead ultimately to dementia. The common point found in all these pathologies is the accumulation in neural and/or glial cells of abnormal forms of Tau protein, leading to its aggregation and neurofibrillary tangles. Zebrafish transgenic models have been generated with different overexpression strategies of human Tau protein. These transgenic lines have made it possible to highlight Tau interacting factors or factors which may limit the neurotoxicity induced by mutations and hyperphosphorylation of the Tau protein in neurons. Several studies have tested neuroprotective pharmacological approaches. On few-days-old larvae, modulation of various signaling or degradation pathways reversed the deleterious effects of Tau mutations, mainly hTauP301L and hTauA152T. Live imaging and live tracking techniques as well as behavioral follow-up enable the analysis of the wide range of Tau-related phenotypes from synaptic loss to cognitive functional consequences.

scholarly journals Business Co-operatives in Australia: “Unlikely Soil for a Co-operative Movement”

2021 ◽  
pp. 1-25
Author(s):  
Greg Patmore ◽  
Nikola Balnave ◽  
Olivera Marjanovic
Keyword(s):  
Business Model ◽  
Common Good ◽  
Business Owners ◽  
The Self ◽  
Small Business Owners ◽  
Large Database ◽  
Average Life ◽  
Direct Competition ◽  
The Common ◽  
Over Time

While co-operatives are traditionally associated with workers, consumers, and farmers, the business model, with its emphasis on democracy and community, has also been adopted by small business owners, the self-employed, and professionals. These business co-operatives are distinct phenomenon, because they primarily consist of independent organizational entities that are not co-operatives and are generally in direct competition with one another. They are unique in that they bring together separate organizations that seek to combat market threats while adopting a philosophy based on co-operative principles. This article begins with an overview of the Australian co-operative landscape. It then defines the concept of business co-operatives and then draws upon the Visual Atlas of Australian Co-operatives History Project, which has developed a large database of Australian co-operatives over time and space, to examine the development of business co-operatives in Australia. It looks at where business co-operatives formed in the economy, the motivation underlying their formation, their average life spans, and their relationships with the broader co-operative movement. The article highlights the value of business co-operatives in introducing the values of participatory democracy and working for the common good into unanticipated markets and reinforcing the co-operative movement.

A comparison of cognitive functioning in acute schizophrenia and depression

2013 ◽  
Vol 25 (6) ◽  
pp. 334-341 ◽  
Author(s):  
Tina Gooren ◽  
Peter Schlattmann ◽  
Peter Neu
Keyword(s):  
Major Depression ◽  
Cognitive Deficits ◽  
Verbal Fluency ◽  
Verbal Learning ◽  
Trail Making Test ◽  
Acute Schizophrenia ◽  
Wechsler Memory Scale ◽  
Schizophrenic Patients ◽  
Trail Making ◽  
Unipolar Major Depression

ObjectiveEven though cognitive deficits are well recognised in schizophrenia and depression, direct comparisons between the disorders are scarce in literature. This study aims to assess specificity and degree of cognitive deficits in inpatients with acute schizophrenia and unipolar major depression.MethodsA neuropsychological test battery was administered to 76 schizophrenic patients, 102 patients with unipolar major depression and 85 healthy controls (HCs), assessing verbal learning [Rey Auditory Verbal Learning Test (RAVLT)], processing speed (Trail Making Test), verbal fluency and visual memory (Wechsler Memory Scale-Revised test).ResultsBoth patient groups were significantly impaired compared with HCs with regard to all test outcomes. The schizophrenia group (SG) performed significantly worse in the Wechsler Memory Scale and verbal fluency than the depression group (DG). The DG reached significantly lower scores than the SG in the RAVLT delayed recall subtest. No significant group difference between SG and DG was found for the Trail Making Test and the RAVLT direct recall trails.ConclusionOur results indicate that cognitive impairment is present in both disorders. Schizophrenic patients performed worse than patients with unipolar depression in only two of the administered tests. Differences in cognitive performance between the groups are not as general as often assumed. Therefore, during the acute phase of illness, a diagnostic classification on the grounds of the patients’ neurocognitive performance has to be done with caution.

Prenatal exposure to lipopolysaccharide results in cognitive deficits in age-increasing offspring rats

Neuroscience ◽  
2010 ◽  
Vol 166 (3) ◽  
pp. 763-770 ◽  
Author(s):  
L.Y. Hao ◽  
X.Q. Hao ◽  
S.H. Li ◽  
X.H. Li
Keyword(s):  
Prenatal Exposure ◽  
Cognitive Deficits

Protective effect of citicoline against aluminum-induced cognitive impairments in rats

2016 ◽  
Vol 33 (4) ◽  
pp. 308-317 ◽  
Author(s):  
Ahmed O Abdel-Zaher ◽  
Mostafa M Hamdy ◽  
Mahran S Abdel-Rahman ◽  
Doaa H Abd El-hamid
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Passive Avoidance ◽  
Morris Water Maze ◽  
Cognitive Deficits ◽  
Aluminum Chloride ◽  
Water Maze ◽  
Cognitive Impairments ◽  
Radial Arm Maze ◽  
Time Required

The potential protective effect of citicoline on aluminum chloride-induced cognitive deficits was investigated in rats. In a Morris water maze, administration of aluminum chloride to rats for 90 days resulted in increased escape latency to reach the platform and decreased swimming speed in acquisition trials. Similarly, in probe trials, the time required to reach the hidden platform was increased and the time spent in the target quadrant was reduced. Also, administration of aluminum chloride to rats for 90 days increased the reference and working memory errors and time required to end the task in the radial arm maze. In addition, this treatment decreased the step-through latency in the passive avoidance test. Concurrently, treatment of rats with aluminum chloride for 90 days increased hippocampal glutamate, malondialdehyde, and nitrite levels and decreased intracellular reduced glutathione level. In the citicoline-treated group, aluminum chloride-induced learning and memory impairments as assessed by the Morris water maze, radial arm maze, and passive avoidance tests were inhibited. At the same time, treatment of rats with citicoline prevented the biochemical alterations induced by aluminum chloride in the hippocampus. It can be concluded that elevation of hippocampal glutamate level with consequent oxidative stress and nitric oxide (NO) overproduction may play an important role in aluminum-induced cognitive impairments. Also, our results suggest, for the first time, that citicoline can protect against the development of these cognitive deficits through inhibition of aluminum-induced elevation of glutamate level, oxidative stress, and NO overproduction in the hippocampus.

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