Relevant bibliographies by topics / Preclinical models of addiction

Academic literature on the topic 'Preclinical models of addiction'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Preclinical models of addiction"

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Singer, Bryan F. "Diverse Characteristics of Addiction Necessitate Multiple Preclinical Models." Biological Psychiatry 86, no. 11 (December 2019): e43-e45. http://dx.doi.org/10.1016/j.biopsych.2019.09.024.

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Yahyavi-Firouz-Abadi, Noushin, and Ronald E. See. "Anti-relapse medications: Preclinical models for drug addiction treatment." Pharmacology & Therapeutics 124, no. 2 (November 2009): 235–47. http://dx.doi.org/10.1016/j.pharmthera.2009.06.014.

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Banks, Matthew L., and S. Stevens Negus. "Insights from Preclinical Choice Models on Treating Drug Addiction." Trends in Pharmacological Sciences 38, no. 2 (February 2017): 181–94. http://dx.doi.org/10.1016/j.tips.2016.11.002.

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Schulteis, Gery, Lisa H. Gold, and George F. Koob. "Preclinical Behavioral Models for Addressing Unmet Needs in Opiate Addiction." Seminars in Neuroscience 9, no. 3-4 (1997): 94–109. http://dx.doi.org/10.1006/smns.1997.0110.

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Peters, Jamie, and David E. Olson. "Engineering Safer Psychedelics for Treating Addiction." Neuroscience Insights 16 (January 2021): 263310552110338. http://dx.doi.org/10.1177/26331055211033847.

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Addiction is best described as a disorder of maladaptive neuroplasticity involving the simultaneous strengthening of reward circuitry that drives compulsive drug seeking and weakening of circuits involved in executive control over harmful behaviors. Psychedelics have shown great promise for treating addiction, with many people attributing their therapeutic effects to insights gained while under the influence of the drug. However, psychedelics are also potent psychoplastogens—molecules capable of rapidly re-wiring the adult brain. The advent of non-hallucinogenic psychoplastogens with anti-addictive properties raises the intriguing possibility that hallucinations might not be necessary for all therapeutic effects of psychedelic-based medicines, so long as the underlying pathological neural circuitry can be remedied. One of these non-hallucinogenic psychoplastogens, tabernanthalog (TBG), appears to have long-lasting therapeutic effects in preclinical models relevant to alcohol and opioid addiction. Here, we discuss the implications of these results for the development of addiction treatments, as well as the next steps for advancing TBG and related non-hallucinogenic psychoplastogens as addiction therapeutics.
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ROTHMAN, RICHARD B., GREGORY I. ELMER, TONI S. SHIPPENBERG, WILLIAM REA, and MICHAEL H. BAUMANN. "Phentermine and Fenfluramine: Preclinical Studies in Animal Models of Cocaine Addiction." Annals of the New York Academy of Sciences 844, no. 1 (May 1998): 59–74. http://dx.doi.org/10.1111/j.1749-6632.1998.tb08222.x.

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Menne, Victoria, and Rose Chesworth. "Schizophrenia and drug addiction comorbidity: recent advances in our understanding of behavioural susceptibility and neural mechanisms." Neuroanatomy and Behaviour 2 (January 16, 2020): e10. http://dx.doi.org/10.35430/nab.2020.e10.

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Schizophrenia is a severe psychiatric disorder which is worsened substantially by substance abuse/addiction. Substance abuse affects nearly 50% of individuals with schizophrenia, extends across several drug classes (e.g. nicotine, cannabinoids, ethanol, psychostimulants) and worsens overall functioning of patients. Prominent theories explaining schizophrenia and addiction comorbidity include the primary addiction hypothesis (i.e. schizophrenia susceptibility primes drug reward circuits, increasing drug addiction risk following drug exposure), the two-hit hypothesis (i.e. drug abuse and other genetic and/or environmental risk factors contribute to schizophrenia development) and the self-medication hypothesis (i.e. drug use alleviates schizophrenia symptoms). Animal models can be used to evaluate the utility and validity of these theories. Since this literature was last reviewed by Ng and colleagues in 2013 [Neurosci Biobehav Rev, 37(5)], significant advances have been made to our understanding of schizophrenia and substance abuse comorbidity. Here we review advances in the field since 2013, focussing on two key questions: 1) Does schizophrenia susceptibility increase susceptibility to drug addiction (assessing the primary addiction hypothesis), and 2) Do abused drugs exacerbate or ameliorate schizophrenia symptoms (assessing the two-hit hypothesis and the self-medication hypothesis). We addressed these questions using data from several schizophrenia preclinical models (e.g. genetic, lesion, neurodevelopmental, pharmacological) across drug classes (e.g. nicotine, cannabinoids, ethanol, psychostimulants). We conclude that addiction-like behaviour is present in several preclinical schizophrenia models, and drugs of abuse can exacerbate but also ameliorate schizophrenia-relevant behaviours. These behavioural changes are associated with altered receptor system function (e.g. dopaminergic, glutamatergic, GABAergic) critically implicated in schizophrenia and addiction pathology.
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McLemon, Erin, and Rose Chesworth. "Cannabinoid treatment of opiate addiction." Neuroanatomy and Behaviour 3 (June 12, 2021): e14. http://dx.doi.org/10.35430/nab.2021.e14.

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Opioid abuse is a growing global problem. Current therapies for opioid abuse target withdrawal symptoms and have several adverse side effects. There are no treatments to address opioid-induced neural adaptations associated with abuse and addiction. Preclinical research demonstrates interactions between the endogenous opioid and cannabinoid systems, suggesting that cannabinoids may be used to treat opioid addiction and dependence. The aim of this review is to assess how cannabinoids affect behavioural and molecular measures of opioid dependence and addiction-like behaviour in animal models. It appears that cannabidiol and cannabinoid receptor 1 (CB1R) antagonists have potential for treating drug-craving and drug-seeking behaviour, based on evidence from preclinical animal models. Ligands which inhibit the action of cannabinoid degradation enzymes also show promise in reducing opioid withdrawal symptoms and opioid self-administration in rodents. Agonists of CB1R could be useful for treating symptoms of opioid withdrawal; however, the clinical utility of these drugs is limited by side effects, the potential for cannabinoid addiction and an increase in opiate tolerance induced by cannabinoid consumption. The mechanisms by which cannabinoids reduce opioid addiction-relevant behaviours include modulation of cannabinoid, serotonin, and dopamine receptors, as well as signalling cascades involving ERK-CREB-BDNF and peroxisome proliferator-activated receptor-α. Identifying the receptors involved and their mechanism of action remains a critical area of future research.
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Duncan, Jhodie R., and Andrew J. Lawrence. "The role of metabotropic glutamate receptors in addiction: Evidence from preclinical models." Pharmacology Biochemistry and Behavior 100, no. 4 (February 2012): 811–24. http://dx.doi.org/10.1016/j.pbb.2011.03.015.

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Belin-Rauscent, Aude, Maxime Fouyssac, Antonello Bonci, and David Belin. "How Preclinical Models Evolved to Resemble the Diagnostic Criteria of Drug Addiction." Biological Psychiatry 79, no. 1 (January 2016): 39–46. http://dx.doi.org/10.1016/j.biopsych.2015.01.004.

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Dissertations / Theses on the topic "Preclinical models of addiction"

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Fouyssac, Maxime. "Behavioural and cellular basis of the vulnerability to develop compulsive heroin seeking habits." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/271886.

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Addiction is a chronic relapsing disorder for which there is no effective treatment. This may reflect our lack of understanding of the psychological and neural mechanisms that support the transition, in vulnerable individuals, from recreational drug use to compulsive drug seeking habits. Over the last decade clinical and preclinical studies have begun to shed light on the psychological and neural basis of the individual vulnerability to cocaine addiction, but despite the epidemic in opiates addiction in the USA and incremental opioid drug abuse and addiction in the UK, heroin addiction has hitherto been under-investigated. Using a novel preclinical model of compulsive heroin seeking behaviour in which some rats self-administering heroin persist in responding under a second-order schedule of reinforcement despite punishment (Chapter 3), the experiments in this thesis investigated the psychological, behavioural, neural and cellular mechanisms involved in the vulnerability to develop compulsive heroin seeking. Chapter 4 aimed to identify behavioural traits, such as anxiety, stress reactivity or decision making, that predict an increased vulnerability to develop compulsive heroin seeking. Chapter 5 aimed to characterise the neural and cellular correlates of heroin seeking habits, and compulsivity. Based on the combination of hotspot analysis, quantitative PCR, RNAscope and western-blot analyses, the data presented demonstrate that compulsive habits are associated with a differential pattern of cellular plasticity within corticostriatal networks, and are preceded by diverse cellular adaptations, especially in the striatum, in vulnerable individuals. Finally, chapter 6 further investigated the cellular specificity of the observed adaptations in experiments that revealed exposure to heroin and cocaine, triggers a downregulation of the dopamine transporter preferentially in astrocytes, and not in neurons as previously thought. The results presented in this thesis offer new insights into the neural and cellular basis of the vulnerability to develop compulsive heroin seeking, a key feature of opioid addiction.
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Zhang, Ting. "DEVELOPMENT AND PRECLINICAL EVALUATION OF LONG-LASTING COCAINE HYDROLASES FOR COCAINE OVERDOSE AND COCAINE USE DISORDER TREATMENT." UKnowledge, 2018. https://uknowledge.uky.edu/pharmacy_etds/93.

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Cocaine is a plant-based illicit drug commonly involved in substance use disorder. Although cocaine overdose and cocaine use disorders cause adverse health consequences to individuals and the economic burden on their family and society, there are no FDA (Food and Drug Administration) approved medications for treatment. Recently, it has been recognized that delivery of cocaine hydrolase (CocH) is a promising therapeutic strategy. Human butyrylcholinesterase (hBChE), the primary enzyme involved in cocaine metabolism in human, have advantages over other candidates for the development of CocH. Previous studies in our laboratory have designed and characterized hBChE mutants that have ~4,000-fold improved catalytic efficiency against naturally occurring (-)-cocaine as compared to the wild-type hBChE. Besides the catalytic efficiency, the biological half-life is another essential factor that influences the desired therapeutic value in the long-term treatment of cocaine use disorder. In order to provide prolonged effects to reduce administration frequency in clinical use, efforts have been made to increase the retention time of CocHs in blood circulation by fusing CocHs with other thermostable proteins or their mutants, including human serum albumin (Albu) or the Fc region of the human IgG (Fc). In this dissertation, we demonstrated the clinical potential and the benefits of long-lasting CocHs for cocaine overdose treatment. We used rodent models to show the ability of AlbuCocH1 to block or reverse manifestations of toxic effects of cocaine. In addition, a concomitant LC-MS/MS-based analysis was conducted to investigate the pharmacokinetic profile of a lethal dose of cocaine with the presence of AlbuCocH1. These experimental data demonstrated AlbuCocH1 as an effective cocaine detoxification agent by accelerating the metabolism of cocaine. In order to examine the potential therapeutic value of Fc-fused CocHs in the treatment of cocaine use disorder, we conducted a series of behavioral experiments in rats to evaluate the effectiveness and duration of Fc-fused CocHs in blocking or attenuating cocaine-induced psychostimulant and discriminative stimulus effects. In addition, the intravenous self-administration model was used to investigate the long-term effectiveness of Fc-fused CocHs in blocking or attenuating the reinforcing effects of cocaine. It has been shown that a single dose of E30-6-Fc (3 mg/kg) was able to effectively alter the cocaine dose-response curve and attenuate the reinforcing efficacy of cocaine for at least a month in both male and female rats. In summary, AlbuCocH1 (TV-1380), which failed to meet the primary efficacy endpoint in clinical trials for facilitating abstinence in cocaine-dependent subjects with a weekly dosing schedule (due to the short biological half-life), is more suitable to be developed as a cocaine detoxification agent. On the contrary, the newly designed Fc-fused CocH (e.g. CocH3-Fc, E30-6-Fc) with higher catalytic efficiency and longer biological half-life will be beneficial for long-term abstinence management in cocaine-dependent individuals.
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Delgado, San Martin Juan A. "Mathematical models for preclinical heterogeneous cancers." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230139.

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Cancer is a deadly, complex disease with 14 million new cases diagnosed every year and the endeavour to develop a cure is a global multidisciplinary effort. The complexity of cancer and the resulting vast volume of data derived from its research necessitates a robust and cutting-edge system of mathematical and statistical modelling. This thesis proposes novel mathematical models of quantification and modelling applied to heterogeneous preclinical cancers, focusing on the translation of animal studies into patients with particular emphasis on tumour stroma. The first section of this thesis (quantification) will present different techniques of extracting and quantifying data from bioanalytical assays. The overall aim will be to present and discuss potential methods of obtaining data regarding tumour volume, stromal morphology, stromal heterogeneity, and oxygen distribution. Firstly, a 3D scanning technique will be discusses. This technique aims to assess tumour volume in mice more precisely than the current favoured method (callipers) and record any cutaneous symptoms as well, with the potential to revolutionise tumour growth analysis. Secondly, a series of image processing methods will be presented which, when applied to tumour histopathology, demonstrate that tumour stromal morphology and its microenvironment play a key role in tumour physiology. Lastly, it will be demonstrated through the integration of in-vitro data from various sources that oxygen and nutrient distribution in tumours is very irregular, creating metabolic niches with distinct physiologies within a single tumour. Tumour volume, oxygen, and stroma are the three aspects central to the successful modelling of tumour drug responses over time. The second section of this thesis (modelling) will feature a mathematical oxygen-driven model - utilising 38 cell lines and 5 patient-derived animal models - that aims to demonstrate the relationship between homogeneous oxygen distribution and preclinical tumour growth. Finally, all concepts discussed will be merged into a computational tumour-stroma model. This cellular automaton (stochastic) model will demonstrate that tumour stroma plays a key role in tumour growth and has both positive (at a molecular level) and negative (at both a molecular and tissue level) effects on cancers. This thesis contains a useful set of algorithms to help visualise, quantify, and understand tissue phenomena in cancer physiology, as well as providing a series of platforms to predict tumour outcome in the preclinical setting with clinical relevance.
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Chaffee, Beth K. "Preclinical Modeling of Musculoskeletal Cancer." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376844544.

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Henkel, Jan. "Bone tissue engineering in two preclinical ovine animal models." Thesis, Queensland University of Technology, 2017. https://eprints.qut.edu.au/109909/1/Jan_Henkel_Thesis.pdf.

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This PhD-research was focused on the development and evaluation of innovative scaffold-based bone tissue engineering concepts for the treatment of large volume bone defects, which still represent a major challenge in orthopaedic and reconstructive surgery. Two different types of bone tissue engineering constructs were investigated and successfully applied to regenerate critically-sized segmental bone defects in ovine animal models. The results outlined in the PhD thesis represent a significant contribution to potential future clinical translations of bone tissue engineering concepts from bench to bedside.
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Ernst, Agnes Stefanie. "Molecular analysis of preclinical models for mental and metabolic disorders." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610813.

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Wetzel, Hanna N. "Preclinical Development of the Anti-cocaine Monoclonal Antibody h2E2 for the Treatment of Cocaine Addiction." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1529333855259163.

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Creedon, Helen. "Use of genetically engineered mouse models in preclinical drug development." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15911.

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The paucity of well validated preclinical models is frequently cited as a contributing factor to the high attrition rates seen in clinical oncological trials. There remains a critical need to develop models which are accurately able to recapitulate the features of human disease. The aims of this study were to use genetically engineered mouse models (GEMMs) to explore the efficacy of novel treatment strategies in HER2 positive breast cancer and to further develop the model to facilitate the study of mechanisms underpinning drug resistance. Using the BLG--HER2KI-PTEN+/- model, we demonstrated that Src plays an important role in the early stages of tumour development. Chemopreventative treatment with dasatinib delayed tumour inititation (p= 0.046, Wilcoxon signed rank test) and prolonged overall survival (OS) (p=0.06, Wilcoxon signed rank test). Dasatinib treatment also induced squamous metaplasia in 66% of drug treated tumours. We used 2 cell lines derived from this model to further explore dasatinib’s mechanism of action and demonstrated reduced proliferation, migration and invasion following in vitro treatment. Due to the prolonged tumour latency and the low metastatic rate seen in this model, further studies were undertaken with the MMTV-NIC model. This model also allowed us to study the impact of PTEN loss on therapeutic response. We validated this model by treating a cohort of MMTV-NIC PTEN+/- mice with paclitaxel and demonstrated prolonged OS (p=0.035, Gehan Breslow Wilcoxon test). AZD8931 is an equipotent signalling inhibitor of HER2, HER3 and EGFR. We observed heterogeneity in tumour response but overall AZD8931 treatment prolonged OS in both MMTV-NIC PTEN FL/+ and MMTV-NIC PTEN+/- models. PTEN loss was associated with reduced sensitivity to AZD8931 and failure to suppress Src activity, suggesting these may be suitable predictive biomarkers of AZD8931 response. To facilitate further studies exploring resistance, we transplanted MMTV-NIC PTEN+/- fragments into syngeneic mice and generated 3 tumours with acquired resistance to AZD8931. These tumours displayed differing resistance strategies; 1 tumour continued to express HER2 whilst the remaining 2 underwent EMT and lost HER2 expression reflecting to a very limited degree some of the heterogeneity of resistance strategies seen in human disease. To further explore resistance to HER2 targeting tyrosine kinase inhibitors, we generated a panel of human cell lines with acquired resistance to AZD8931 and lapatinib. Western blotting demonstrated loss of HER2, HER3 and PTEN in all resistant lines. Acquisition of resistance was associated with a marked change in phenotype and western blotting confirmed all lines had undergone EMT. We used a combination of RPPA and mass spectrometry to further characterise the AZD8931 resistant lines and identified multiple potential novel proteins involved in the resistant phenotype, including several implicated in EMT. In conclusion, when coupled with appropriate in vitro techniques, the MMTV-NIC model is a valuable tool for selection of emerging drugs to carry forward into clinical trials of HER2 positive breast cancer.
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Precazzini, Francesca. "Zebrafish models of uveal and cutaneous melanoma for preclinical studies." Doctoral thesis, Università degli studi di Trento, 2019. http://hdl.handle.net/11572/245749.

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Uveal melanoma (UM) is the most common primary cancer of the eye and its prognosis is strongly influenced by the occurrence of metastases, which are both rapidly developing and mostly fatal. The most frequent driver mutations occur in a small number of genes including GNAQ, GNA11, BAP1, CYSLTR2 and SF3B1. Due to a lack of suitable animal models, the mechanism through which mutations in these genes cause or cooperate in UM initiation and progression is still largely unknown. We aimed at generating transgenic strains expressing the human mutant proteins in zebrafish uveal melanocytes, using the kita promoter. We used the binary Gal4/UAS system to express the mutant genes mentioned above. Moreover, we performed xenotransplantation experiments with uveal melanoma human and zebrafish cell lines in optically-clear, immunocompromised, zebrafish larvae. Transplanted fish developed melanoma near the site of transplantation in two weeks and showed metastatic growth within one month of age. This approach could be used for short-term assays in larvae, and be further developed for long-term uveal melanoma studies. In parallel, we performed a chemical screen using a transgenic model previously generated in our laboratory, where oncogenic RAS is expressed under the kita promoter. As adults transgenic kita:RAS develop cutaneous melanoma with high frequency and uveal melanoma with a much lower percentage. Larvae showed an increased number of melanocytes already at 3 days post fertilization (dpf) as the earliest evidence of abnormal melanocyte growth. Using this model we performed a chemical screen based on automated detection of a reduction of melanocytes number caused by any of the 1280 FDA or EMA approved drugs of the Prestwick library. The analysis showed that 55 molecules were able to reduce by 60% or more the number of melanocytes per embryo. We identified clotrimazole, as the best candidate. The molecule is an azole derivative acting on the energetic metabolism of melanoma cells. We further tested two compounds for each of the 5 pharmacological classes, and a farnesyltransferase inhibitor (lonafarnib), that inhibits an essential post-translational modification of HRAS and suppresses the hyperpigmentation phenotype. Combinations of clotrimazole and lonafarnib showed the most promising results in zebrafish embryos, allowing a dose reduction of both drugs. We performed validation of these observations in the metastatic human melanoma cell line A375M, and in normal human epithelial melanocytes (NHEM) as control cells, in order to investigate the mechanism of action of clotrimazole in blocking the proliferation of transformed melanocytes. Viability assay and analysis of energy metabolism in clotrimazole treated cells show that this drug specifically affects melanoma cells in vitro and transformed melanocytes in vivo, having no effects on NHEM or wild type larvae. Similar effects were observed with another hit of the antifungal class, miconazole. Furthermore, we show that the effects of clotrimazole are mediated by the inhibition of hexokinase activity and suggest further testing of clotrimazole in combinatorial treatments. In conclusion, this thesis investigated different possibilities of modeling the rare cancer uveal melanoma in zebrafish, using both transgenic and transplantation approaches, and developed a pipeline for a high-throughput, semi-automated chemical screen in a zebrafish melanoma that identified clotrimazole and miconazole as targeting a metabolic vulnerability in melanoma cells.
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Samtani, Grace, and Grace Samtani. "Evaluation of Drug "X" in Preclinical Models of Parkinson's Disease." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625144.

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Parkinson's disease (PD) is a hypokinetic, age-related movement disorder associated with chronic, progressive degeneration of dopaminergic neurons, with cell bodies located in the substantia nigra pars compacta (SNpc) and axon terminals in the striatum. Striatal depletion of the neurotransmitter dopamine (DA) gives rise to the cardinal PD motor symptoms. We utilized a 6-hydroxydopamine (6-OHDA) animal PD model to test the application of a preclinical drug candidate, drug "X", in ameliorating and/or preventing advanced parkinsonism in two studies. First, a neurorestoration study tested the efficacy of drug "X" in restoring motor functionality to animals in which the 6-OHDA lesion had fully developed. Second, a neuroprotection study assessed the effectiveness of drug "X" in preventing the initial development of the 6-OHDA lesion and the onset of motor impairments. Behavioral data indicate that there are no significant differences between the control and drug "X" groups in both studies, suggesting that drug "X" does not improve established severe PD motor deficits nor prevent their initial development. However, we are analyzing brain tissue harvested to 1) verify the extent of the lesion with stereology in the SNpc, 2) evaluate striatal DA levels, and 3) investigate any neuroprotective effects of drug "X" on nigral DAergic neurons.
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Books on the topic "Preclinical models of addiction"

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Aguilar, María A., ed. Methods for Preclinical Research in Addiction. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1748-9.

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Guest, Paul C., ed. Clinical and Preclinical Models for Maximizing Healthspan. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0471-7.

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1948-, Gad Shayne C., ed. Preclinical development handbook. Hoboken, N.J: John Wiley & Sons, 2008.

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Boulton, Alan A., Glen B. Baker, and Peter H. Wu. Animal Models of Drug Addiction. New Jersey: Humana Press, 1992. http://dx.doi.org/10.1385/0896032175.

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Olmstead, Mary C., ed. Animal Models of Drug Addiction. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-934-5.

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Tuli, Hardeep Singh, ed. Drug Targets in Cellular Processes of Cancer: From Nonclinical to Preclinical Models. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7586-0.

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AAG/NIDA Symposium (2006 Chicago, Ill.). Geography and drug addiction. Edited by Thomas Yonette F, Richardson Douglas 1950-, Cheung Ivan, Association of American Geographers, and National Institute on Drug Abuse. [Dordrecht]: Springer, 2008.

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F, Thomas Yonette, Richardson Douglas 1950-, Cheung Ivan, Association of American Geographers, and National Institute on Drug Abuse, eds. Geography and drug addiction. [Dordrecht]: Springer, 2008.

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Becker, Gary Stanley. An empirical analysis of cigarette addiction. Cambridge, MA: National Bureau of Economic Research, 1990.

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S, Olton David, Gamzu Elkan 1943-, Corkin Suzanne, and New York Academy of Sciences., eds. Memory dysfunctions: An integration of animal and human research from preclinical and clinical perspectives. New York, N.Y: New York Academy of Sciences, 1985.

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Book chapters on the topic "Preclinical models of addiction"

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Monleón, Santiago, Rosa Redolat, Aránzazu Duque, Patricia Mesa-Gresa, and Concepción Vinader-Caerols. "Animal Models of Adolescent Binge Drinking." In Methods for Preclinical Research in Addiction, 21–45. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1748-9_2.

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Borruto, Anna Maria, Ana Domi, Laura Soverchia, Esi Domi, Hongwu Li, and Nazzareno Cannella. "Preclinical Models of Relapse to Psychostimulants Induced by Environmental Stimuli." In Methods for Preclinical Research in Addiction, 173–95. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1748-9_7.

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Wilkinson, Courtney, Harrison Blount, Lori Knackstedt, and Marek Schwendt. "Investigation of Individual Differences in Stress Susceptibility and Drug-Seeking in an Animal Model of SUD/PTSD Comorbidity." In Methods for Preclinical Research in Addiction, 247–64. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1748-9_10.

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Cuadrado, Irene, Jesús Egido, Jose Luis Zamorano, and Carlos Zaragoza. "Preclinical Models." In Handbook of Small Animal Imaging, 35–47. Boca Raton: Taylor & Francis, 2016. | Series: Imaging in medical diagnosis and therapy: CRC Press, 2018. http://dx.doi.org/10.1201/9781315373591-4.

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Spanagel, Rainer. "To Open Up New Vistas in Basic and Preclinical Addiction Research." In Addiction Medicine, 1507–23. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0338-9_75.

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Huang, Weihua, Wenhao Xu, and Ming D. Li. "Mouse Models: Knockouts/Knockins." In Addiction Medicine, 181–99. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0338-9_9.

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Fraser, Suzanne, David Moore, and Helen Keane. "Models of Addiction." In Habits: Remaking Addiction, 26–59. London: Palgrave Macmillan UK, 2014. http://dx.doi.org/10.1057/9781137316776_2.

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Fuso Nerini, Ilaria, and Roberta Frapolli. "Preclinical Models in Mesothelioma." In Mesothelioma, 85–98. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16884-1_6.

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Mika, Joanna, Wioletta Makuch, and Barbara Przewlocka. "Preclinical Cancer Pain Models." In Cancer Pain, 71–93. London: Springer London, 2013. http://dx.doi.org/10.1007/978-0-85729-230-8_6.

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Cheng, Menglin, and Kristine Glunde. "Magnetic Resonance Spectroscopy Studies of Mouse Models of Cancer." In Preclinical MRI, 331–45. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7531-0_20.

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Conference papers on the topic "Preclinical models of addiction"

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Eads, Jennifer, Yiqing Zhao, David Bajor, and Zhenghe John Wang. "Abstract PR09: Targeting glutamine addiction of PIK3CA mutant colorectal cancers: From preclinical models to clinical trials." In Abstracts: AACR Special Conference on Targeting PI3K/mTOR Signaling; November 30-December 8, 2018; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.pi3k-mtor18-pr09.

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Zhao, Yiqing, Jennifer Eads, David Bajor, and zhenghe wang. "Abstract LB-294: Targeting glutamine addiction of PIK3CA mutant colorectal cancers: From preclinical models to clinical trials." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-lb-294.

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Zhao, Yiqing, Jennifer Eads, David Bajor, and zhenghe wang. "Abstract LB-294: Targeting glutamine addiction of PIK3CA mutant colorectal cancers: From preclinical models to clinical trials." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-lb-294.

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Trachet, Erin, and Maryland Rosenfeld Franklin. "Abstract 36: Preclinical models of multiple myeloma." In Abstracts: Second AACR Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; May 6-9, 2017; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.hemmal17-36.

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Bouvet, Michael, and Robert M. Hoffman. "Preclinical fluorescent mouse models of pancreatic cancer." In Biomedical Optics (BiOS) 2007, edited by Samuel Achilefu, Darryl J. Bornhop, Ramesh Raghavachari, Alexander P. Savitsky, and Rebekka M. Wachter. SPIE, 2007. http://dx.doi.org/10.1117/12.708060.

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Duchamp, Olivier, Gael Krysa, Robin Artus, Hugo Quillery, Maxime Ramelet, Valerie Boullay, Laure Levenez, et al. "Abstract 5638: Liver preclinical models - acute, chronic and cancer models." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5638.

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Hedberg, Matthew Louis, Hua Li, Yan Zeng, and Jennifer Rubin Grandis. "Abstract A39: PI3K inhibition in preclinical models of HNSCC." In Abstracts: AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; September 14-17, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.pi3k14-a39.

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Rosen, JM. "Abstract DL-1: Leveraging Preclinical Models of Breast Cancer." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-dl-1.

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Arifler, Dizem, and Martial Guillaud. "Identification of azimuthal light scattering signatures to selectively track changes in subnuclear refractive index profile of epithelial cell models." In Preclinical and Clinical Optical Diagnostics, edited by J. Quincy Brown and Ton G. van Leeuwen. SPIE, 2019. http://dx.doi.org/10.1117/12.2526727.

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Srivastava, Apurva K., Melinda G. Hollingshead, Jeevan P. Govindharajulu, Joseph M. Covey, Dane Liston, James Peggins, Donald P. Bottaro, et al. "Abstract 3691: Met target inhibition-guided efficacy in preclinical models." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3691.

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Reports on the topic "Preclinical models of addiction"

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Shannon, Kevin M., Andrea McClatchey, Luis Parada, Marco Giovanni, and Tylr Jack. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada404608.

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Shannon, Kevin M., Andrea McClatchey, Luis Parada, Marco Giovannini, Tyler Jacks, and Judy Small. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada444651.

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Shannon, Kevin M. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada431974.

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Shannon, Kevin, Andrea McClatchey, Luis Parada, Marco Giovannini, and Tylr Jacks. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada411721.

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Shannon, Kevin. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada516646.

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Shannon, Kevin M., Andrea McClatchey, Luis Parada, Marco Giovannini, and Tyler Jacks. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, November 2003. http://dx.doi.org/10.21236/ada425805.

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Shannon, Kevin. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada463499.

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Shannon, Kevin. Preclinical Mouse Models of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada477972.

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Vlad, Anda. Disease Heterogeneity and Immune Biomarkers in Preclinical Mouse Models of Ovarian Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada568359.

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Gregerson, Karen A. Human-Compatible Animal Models for Preclinical Research on Hormones in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada574629.

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