Relevant bibliographies by topics / Dopaminergic dysfunction

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Dopaminergic dysfunction'

Author: Grafiati
Published: 7 June 2025
Last updated: 17 July 2025

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Journal articles on the topic "Dopaminergic dysfunction"

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&NA;. "Glutamatergic modulation of dopaminergic dysfunction." Inpharma Weekly &NA;, no. 1313 (2001): 7. http://dx.doi.org/10.2165/00128413-200113130-00020.

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Thibaut, F., J. M. Ribeyre, and M. Petit. "Dopaminergic dysfunction in deficit syndrome." Biological Psychiatry 42, no. 1 (1997): 203S. http://dx.doi.org/10.1016/s0006-3223(97)87750-5.

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McGowan, Stephen, Andrew D. Lawrence, Tim Sales, Digby Quested, and Paul Grasby. "Presynaptic Dopaminergic Dysfunction in Schizophrenia." Archives of General Psychiatry 61, no. 2 (2004): 134. http://dx.doi.org/10.1001/archpsyc.61.2.134.

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Vidailhet, Marie, Corinne Dupel, Stéphane Lehéricy, et al. "Dopaminergic Dysfunction in Midbrain Dystonia." Archives of Neurology 56, no. 8 (1999): 982. http://dx.doi.org/10.1001/archneur.56.8.982.

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Bykov, Yu V., and V. A. Baturin. "Disruption of the dopaminergic system in the pathophysiology of diabetes mellitus." Ural Medical Journal 22, no. 4 (2023): 119–27. http://dx.doi.org/10.52420/2071-5943-2023-22-4-119-127.

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Introduction. Diabetes mellitus (DM) is the most common endocrinopathy with a high incidence and a high number of complications.The aim of this work was to conduct an analytical literature review assessing the state of the problem of dopaminergic dysfunction in diabetes from a pathophysiological perspective.Materials and methods. Searching Cochrane Library, PubMed, eLibrary, Medscape databases and digital libraries using the search words: diabetes mellitus, dopamine, insulin, dopaminergic system, diabetic encephalopathy. A total of 66 sources were selected for the review.Results and discussion. Dopaminergic system dysfunction can be considered an important component of the pathophysiology of diabetes. Hyperactivation of dopamine (DA) production in the setting of diabetes inhibits insulin synthesis, resulting in hyperglycemia. On the other hand, hypoinsulinemia triggers activation of the dopaminergic system, forming a vicious circle. Increased DA production in diabetes plays an important role in the development of secondary central nervous system dysfunction, primarily through the development of cerebral insufficiency. Numerous preclinical studies confirm the dysfunction of the dopaminergic system (its activation) in diabetes. Clinical studies on this issue are scarce and require further investigation.Conclusion. Dysfunction of the dopaminergic system in diabetes is an important area of research into the pathophysiology of symptomatic neurological disorders in this disease. Type 1 and type 2 diabetes are pathogenetically different diseases, and therefore impaired DA production may be due to insulin deficiency in patients with type 1 diabetes, different timing of manifestation, with hyperinsulinemia and insulin resistance in type 2 diabetes. Finding reliable methods to diagnose dysfunction of the dopaminergic system may improve understanding of the ongoing pathological processes in the neuroendocrine system in diabetes, which is important in addressing their correction in addition to pathogenetic therapy.
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Pignalosa, Francesca Chiara, Antonella Desiderio, Paola Mirra, et al. "Diabetes and Cognitive Impairment: A Role for Glucotoxicity and Dopaminergic Dysfunction." International Journal of Molecular Sciences 22, no. 22 (2021): 12366. http://dx.doi.org/10.3390/ijms222212366.

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Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia, responsible for the onset of several long-term complications. Recent evidence suggests that cognitive dysfunction represents an emerging complication of DM, but the underlying molecular mechanisms are still obscure. Dopamine (DA), a neurotransmitter essentially known for its relevance in the regulation of behavior and movement, modulates cognitive function, too. Interestingly, alterations of the dopaminergic system have been observed in DM. This review aims to offer a comprehensive overview of the most relevant experimental results assessing DA’s role in cognitive function, highlighting the presence of dopaminergic dysfunction in DM and supporting a role for glucotoxicity in DM-associated dopaminergic dysfunction and cognitive impairment. Several studies confirm a role for DA in cognition both in animal models and in humans. Similarly, significant alterations of the dopaminergic system have been observed in animal models of experimental diabetes and in diabetic patients, too. Evidence is accumulating that advanced glycation end products (AGEs) and their precursor methylglyoxal (MGO) are associated with cognitive impairment and alterations of the dopaminergic system. Further research is needed to clarify the molecular mechanisms linking DM-associated dopaminergic dysfunction and cognitive impairment and to assess the deleterious impact of glucotoxicity.
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Pavăl, Denis. "A Dopamine Hypothesis of Autism Spectrum Disorder." Developmental Neuroscience 39, no. 5 (2017): 355–60. http://dx.doi.org/10.1159/000478725.

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Autism spectrum disorder (ASD) comprises a group of neurodevelopmental disorders characterized by social deficits and stereotyped behaviors. While several theories have emerged, the pathogenesis of ASD remains unknown. Although studies report dopamine signaling abnormalities in autistic patients, a coherent dopamine hypothesis which could link neurobiology to behavior in ASD is currently lacking. In this paper, we present such a hypothesis by proposing that autistic behavior arises from dysfunctions in the midbrain dopaminergic system. We hypothesize that a dysfunction of the mesocorticolimbic circuit leads to social deficits, while a dysfunction of the nigrostriatal circuit leads to stereotyped behaviors. Furthermore, we discuss 2 key predictions of our hypothesis, with emphasis on clinical and therapeutic aspects. First, we argue that dopaminergic dysfunctions in the same circuits should associate with autistic-like behavior in nonautistic subjects. Concerning this, we discuss the case of PANDAS (pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections) which displays behaviors similar to those of ASD, presumed to arise from dopaminergic dysfunctions. Second, we argue that providing dopamine modulators to autistic subjects should lead to a behavioral improvement. Regarding this, we present clinical studies of dopamine antagonists which seem to have improving effects on autistic behavior. Furthermore, we explore the means of testing our hypothesis by using neuroreceptor imaging, which could provide comprehensive evidence for dopamine signaling dysfunctions in autistic subjects. Lastly, we discuss the limitations of our hypothesis. Along these lines, we aim to provide a dopaminergic model of ASD which might lead to a better understanding of the ASD pathogenesis.
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Muñoz, Patricia, Sandro Huenchuguala, Irmgard Paris, and Juan Segura-Aguilar. "Dopamine Oxidation and Autophagy." Parkinson's Disease 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/920953.

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The molecular mechanisms involved in the neurodegenerative process of Parkinson's disease remain unclear. Currently, there is a general agreement that mitochondrial dysfunction,α-synuclein aggregation, oxidative stress, neuroinflammation, and impaired protein degradation are involved in the neurodegeneration of dopaminergic neurons containing neuromelanin in Parkinson's disease. Aminochrome has been proposed to play an essential role in the degeneration of dopaminergic neurons containing neuromelanin by inducing mitochondrial dysfunction, oxidative stress, the formation of neurotoxicα-synuclein protofibrils, and impaired protein degradation. Here, we discuss the relationship between the oxidation of dopamine to aminochrome, the precursor of neuromelanin, autophagy dysfunction in dopaminergic neurons containing neuromelanin, and the role of dopamine oxidation to aminochrome in autophagy dysfunction in dopaminergic neurons. Aminochrome induces the following: (i) the formation ofα-synuclein protofibrils that inactivate chaperone-mediated autophagy; (ii) the formation of adducts withα- andβ-tubulin, which induce the aggregation of the microtubules required for the fusion of autophagy vacuoles and lysosomes.
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Ruan, Zhengzheng, Dongdong Zhang, Ruixue Huang, et al. "Microglial Activation Damages Dopaminergic Neurons through MMP-2/-9-Mediated Increase of Blood-Brain Barrier Permeability in a Parkinson’s Disease Mouse Model." International Journal of Molecular Sciences 23, no. 5 (2022): 2793. http://dx.doi.org/10.3390/ijms23052793.

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Chronic neuroinflammation has been considered to be involved in the progressive dopaminergic neurodegeneration in Parkinson’s disease (PD). However, the mechanisms remain unknown. Accumulating evidence indicated a key role of the blood–brain barrier (BBB) dysfunction in neurological disorders. This study is designed to elucidate whether chronic neuroinflammation damages dopaminergic neurons through BBB dysfunction by using a rotenone-induced mouse PD model. Results showed that rotenone dose-dependently induced nigral dopaminergic neurodegeneration, which was associated with increased Evans blue content and fibrinogen accumulation as well as reduced expressions of zonula occludens-1 (ZO-1), claudin-5 and occludin, three tight junction proteins for maintaining BBB permeability, in mice, indicating BBB disruption. Rotenone also induced nigral microglial activation. Depletion of microglia or inhibition of microglial activation by PLX3397 or minocycline, respectively, greatly attenuated BBB dysfunction in rotenone-lesioned mice. Mechanistic inquiry revealed that microglia-mediated activation of matrix metalloproteinases-2 and 9 (MMP-2/-9) contributed to rotenone-induced BBB disruption and dopaminergic neurodegeneration. Rotenone-induced activation of MMP-2/-9 was significantly attenuated by microglial depletion and inactivation. Furthermore, inhibition of MMP-2/-9 by a wide-range inhibitor, SB-3CT, abrogated elevation of BBB permeability and simultaneously increased tight junctions expression. Finally, we found that microglial depletion and inactivation as well as inhibition of MMP-2/-9 significantly ameliorated rotenone-elicited nigrostriatal dopaminergic neurodegeneration and motor dysfunction in mice. Altogether, our findings suggested that microglial MMP-2/-9 activation-mediated BBB dysfunction contributed to dopaminergic neurodegeneration in rotenone-induced mouse PD model, providing a novel view for the mechanisms of Parkinsonism.
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Al-Adawi, S., G. S. Dawe, and A. A. Al-Hussaini. "Aboulia: neurobehavioural dysfunction of dopaminergic system?" Medical Hypotheses 54, no. 4 (2000): 523–30. http://dx.doi.org/10.1054/mehy.1999.0890.

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Dissertations / Theses on the topic "Dopaminergic dysfunction"

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Walls, Brittany D. "NEUROPSYCHOLOGICAL CORRELATES OF STRIATAL DOPAMINERGIC DYSFUNCTION IN PARKINSON’S DISEASE." UKnowledge, 2019. https://uknowledge.uky.edu/psychology_etds/171.

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Parkinson’s disease (PD) is a common neurodegenerative disorder associated with dysfunction of the basal ganglia, which contributes to a range of motor, cognitive, and affective symptoms. Striatal dopaminergic deficits are one of the core pathological mechanisms thought to contribute to the extra-motor (i.e., cognitive and affective) symptoms in early PD. The present study investigated the relationship between striatal dopaminergic integrity and cognition in 21 patients with PD and 21 age and education matched controls. Each individual underwent dopamine transporter (DaT) imaging with single photon emission computed tomography (SPECT) (i.e., DaTscan) and standardized neuropsychological testing. Strong positive associations were found between DaT availability in the striatum and verbal memory (r = .52-.61) and problem solving/set-shifting (r = .55) in patients with PD. Additional moderate to strong positive associations (r = .49-.56) between DaT concentrations and visuospatial functions in patients with PD were found. However, similar significant associations between DaT and cognition were observed in age and education matched controls. Clinically, it is important for health care professionals to consider the role of both striatal and extra-striatal mechanisms as they relate to cognition in PD. Future studies examining the full range of pathological mechanisms that contribute to cognitive dysfunction in PD over time are warranted in order to inform more effective and targeted interventions.
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Paß, Thomas [Verfasser], Peter [Gutachter] Kloppenburg, Aleksandra [Gutachter] Trifunovic, Elena [Gutachter] Rugarli, and Rudolf [Gutachter] Wiesner. "Mitochondrial Dysfunction in Dopaminergic Neurons and the Impact on Neurodegeneration in Parkinson's disease / Thomas Paß ; Gutachter: Peter Kloppenburg, Aleksandra Trifunovic, Elena Rugarli, Rudolf Wiesner." Köln : Universitäts- und Stadtbibliothek Köln, 2020. http://d-nb.info/122042269X/34.

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Dettling, Michael. "Die klinische Relevanz von State-, Trait- und Residualmarkern für die biologische Psychiatrie am Beispiel neuroendokriner und pharmakogenetischer Befunde." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/13743.

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Die Habilitationsschrift beinhaltet eine zusammenfassende Darstellung unterschiedlicher Marker der biologischen Psychiatrie. Hierzu wurden mittels neuroendokriner und molekulargenetischer Verfahren depressive Patienten, alkoholabhängige Patienten und schizophrene Patienten mit einer seltenen Arzneimittelnebenwirkung untersucht und die jeweiligen Befunde als State- Trait- und Residualmarker charakterisiert. Im Bereich Neuroendokrinologie wurden der Dex/CRH-Test und Liquoruntersuchungen bei depressiven Patienten und die Apomorphin-induzierte HGH-Sekretion bei alkoholabhängigen Patienten durchgeführt. Im Bereich Pharmakogenetik erfolgten molekularbiologische HLA-und Enzymsystemuntersuchungen bei Patienten mit einer Clozapin-induzierten Agranulocytose. Es zeigten sich folgende Charakterisierungen einzelner Substrate: * HHN-Systemveränderungen (messbar über Cortisol- und ACTH-Serumkonzentrationen) sind State-bzw. Residualmarker der Depression. CRH-, AVP-und Somatostatin-Liquorkonzentrationen sind keine biologischen Marker der Depression * Das HGH-"Blunting" alkoholabhängiger Patienten ist ein spezifischer Marker für Alkoholabhängigkeit mit ungünstigem klinischen Verlauf * Spezifische HLA-Haplotypen sind als Traitmarker der Clozapin-induzierten Agranulocytose zu werten. Enzymsystem-Polymorphismen haben keine Bedeutung bei der Entwicklung dieser Arzneimittelnebenwirkung Der spezifischen Charakterisierung einzelner Befunde schließt sich eine Diskussion über deren Bedeutung für die biologische Psychiatrie an.<br>Neuroendocrine and pharmacogenetic studies were performed in depressive and alcohol-dependent patients as well as schizophrenic patients with clozapine-induced agranulocytosis to characterize different serological or molecular substrates as state-, trait or residualmarker. Depressive patients were assessed using the dexamethasone/corticotropin releasing hormone test and measuring neuropeptide hormone concentrations in cerebrospinal fluid (CSF), whereas dopaminergic responsiveness of alcohol-dependant patients was assessed by the apomorphine-induced human growth hormone (HGH) secretion. HLA-subtyping and screening of relevant polymorphisms of clozapine metabolizing enzyme systems was performed in patients with clozapine-induced agranulocytosis (CA). * HPA-alterations as a function of cortisol-and ACTH serum concentration appear as state- and residual marker of depression. CSF-CRH, -AVP and -SOM do not fulfill marker criteria * HGH blunting may serve as a residual marker of alcoholism with poor clinical outcome * HLA alleles but not polymorphisms of clozapine metabolizing enzyme systems are associated with CA and thus, underline the importance of imunogenetic mechanisms in the pathophysiology of this idiosyncratic drug reaction. In conclusion, the importance of biological markers for psychiatric research and future directions are discussed
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FERNANDEZ, ABASCAL JESUS. "Role of cytochrome P450 against toxic insult in neuroblastoma SH-SY5Y cells." Doctoral thesis, Università di Siena, 2018. http://hdl.handle.net/11365/1051261.

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Cytochrome P450 (CYP) is one of the main metabolic systems involved in xenobiotic clearance in live organisms. Its activity is mainly carried out at hepatic level, but in the last two decades, its function has been also reported to be important in other extrahepatic tissues, especially in the central nervous system. In brain, CYP isoenzymes vary their expression depending on the brain area and the cell type. However, the role of the different isoforms is not yet well characterized. Some of them have been involved in detoxification and/or toxic activation of xenobiotics; while other have been related with production of oxidative stress through the metabolism of endogenous compounds. Therefore, the presence and the function of the CYP in the brain has been related with neurodegenerative diseases such as Parkinson’s Disease (PD). On the other hand, the study of the degeneration of dopaminergic neurons in vitro has been carried out by the use of several toxins that promote apoptosis and similar pathological features that the observed in PD. Among these xenobiotics, 1-methyl-4-phenylpyridinium (MPP+), rotenone, and paraquat are the most used because they are able to promote neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it has been reported that some CYP isoforms, such as CYP 2D6, can be involved in the development of this neurodegenerative disease. To better characterize this role, we have studied the induction of some isoforms in an in vitro system. Undifferentiated SH-SY5Y cells were treated with well-known inducers of CYP for 48 hours, namely β-naphtoflavone (β-NF), ethanol (EtOH), and cyclophosphamide (CPA); and qRT-PCR, Western Blot (WB) and confocal microscopy analysis were performed. CPA increased the mRNA levels of CYP 1A1, 2D6 and 2E1, while the other inducers promoted a slight increase on these isoforms compared to CPA. WB analysis confirmed the induction promoted by CPA in CYP 1A1 and 2D6, and revealed that CYP 2D6 was also inducible by EtOH. Moreover, CYP 2E1 was increased by β-NF and EtOH treatments. In differentiated SH-SY5Y cells, a preliminary WB analysis of CYP 2D6 and 2E1 was also performed. The results suggested a change in the regulation of the expression of CYP 2D6 when treated with β-NF, and also of CYP 2E1 levels when treated with β-NF and CPA. Immunohistochemistry analysis confirmed the inducibility of CYPs and showed a co-localization of CYP 2D6 with mitochondria. These data indicate that CYP can be induced in both undifferentiated and differentiated neuroblastoma cells, and underline the possibility to use this in vitro system for studying the role of CYPs in neurodegeneration. Moreover, as showed by our group and others, β-naphtoflavone and ethanol have the ability to induce the expression of some CYP isoforms. In order to study the possible role of CYP induction in neurodegeneration, we have use the same in vitro model than before, where undifferentiated neuroblastoma SH-SY5Y cells have been treated with these inducers separately previous and during exposure of MPP+. In both experimental conditions, the toxic effect of MPP+ was partially reverted. MTT assays showed an increase in cell viability of approximately 17% in β-NF treatment, while EtOH showed an increase between 13-15%. The analysis of apoptotic population by flow cytometry showed that both treatments were able to restore the populations to control values compared to the toxic effect of MPP+. The mitochondrial fission-fusion kinetics revealed that both treatments were able to avoid the impairment of this mitochondrial motility after exposure to the toxin. Finally, this neuroprotection was confirmed by a lowest effect of MPP+ upon complex I activity when cells were preincubated with the inducers. These results bring new insights about the possible role of CYPs, specially CYP 2D6, in neuroprotection and possible development of therapeutic drugs.
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McGuinness, Bernadette. "A comparative study on measures of executive dysfunction and attention in Alzheimer's Disease (AD) and vascular dementia (VaD), and influence of genetic variation in apolipoprotein E and dopaminergic systems on these measures." Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437742.

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Söderlund, Göran. "Noise improves cognitive performance in children with dysfunctional dopaminergic neurotransmission /." Stockholm : Department of Psychology, Stockholm University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7040.

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Fuqua, Joshua Lee. "STUDIES OF THE EFFECTS OF DOPAMINE NEURON STIMULATING PEPTIDES IN RODENT MODELS OF NORMAL AND DYSFUNCTIONAL DOPAMINERGIC SYSTEMS." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/90.

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A theoretical post-translational processing model of the proprotein form of glial cell line-derived neurotrophic factor (GDNF) likely produces three biologically active peptides. The three prospective peptides formed are 5, 11, and 17 amino acid peptides, entitled dopamine neuron stimulating peptide -5 (DNSP-5), -11 (DNSP-11), and -17 (DNSP-17), respectively. The DNSPs were hypothesized to increase dopaminergic neuron function because of their relationship to GDNF: a molecule with established neurotrophic actions on dopaminergic neurons. The DNSPs have the potential to provide a therapeutic molecule similar to GDNF, but with increased ease of delivery and improved bioavailability. Neurochemical effects of DNSPs were examined in the nigrostriatal pathway of normal Fischer 344 rats, and DNSP-11 was found to be the most effective in increasing dopamine neurochemical function. Striatal microdialysis, four weeks after a single intranigral administration of DNSP-11, showed significant increases in the baseline concentrations of dopamine, DOPAC, and HVA. In addition, both, potassium and d-amphetamine-evoked dopamine overflow were significantly increased. DNSP-11 was delivered intranigrally to aged Fischer 344 rats to examine DNSP-11’s ability to improve dopaminergic function in aged dopamine neurons. DNSP-11 affected striatal dopaminergic function 28 days after treatment by decreasing baseline concentrations of dopamine and evoked dopamine release. Investigation of DNSP-11 continued, using two models of neurotoxin-induced dopamine neuron loss that model cell loss associated with Parkinson’s disease. The neuroprotective properties of DNSP-11 were evaluated by delivering DNSP-11 prior to the neurotoxic insult. DNSP-11 treatment was unable to protect dopaminergic neurons, but significantly increased dopamine metabolism. In a model of severe dopamine neuron loss, DNSP-11 treatment significantly improved apomorphine-induced rotation behavior, indicative of alterations in the function of nigrostriatal dopaminergic neurons. Subsequent examination of dopamine content within the SN revealed significant increases in dopamine and DOPAC levels by DNSP-11. Taken together, DNSP-11 treatments modified dopamine neurochemistry in all investigated rodent models. The observed long-term alterations of dopamine neurochemistry by DNSP-11 and subsequent behavioral changes support a potential use for DNSP-11 as a therapeutic for dopaminergic cell loss. Increased dopaminergic function by DNSP-11 is evidence for the novel concept that peptides contained within the prodomain of trophic factors can have neurotrophic actions.
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Chen, Shiang-Jiun, and 陳香君. "Neuroelectrophysiological Evaluation of the Sensorimotor System in Dopaminergic Nigrostriatal Dysfunction." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/75656118051169611084.

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碩士<br>高雄醫學大學<br>醫學研究所<br>89<br>Abstract Depletion of striatal dopamine secondary to degeneration of dopaminergic neurons within the substantia nigra is the main cause of Parkinson's disease (PD). The movement disorders in PD patients is related to their inability to generate the appropriate motor command and to build up the premovement facilitation of the motor system. As the sensory input might be used to initiate, control, or monitor ongoing movement, an altered sensorimotor integration due to the impairment of the nigrostriatal dopaminergic pathway has been thought to be partly responsible for their motor deficits. In this respect, it has been suggested that evoked potential recording might display some differences from healthy controls. Therefore, the aim of this study is to examine the possible contribution of noninvasive neuroelectrophysiological methods in evaluating the functionality of sensorimotor integration mechanisms in (predominantly) unilateral PD patients. The techniques of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) that provide information on the transmission of afferent and efferent pathways respectively were used in the present study. SEPs reflect the electric brain potentials elicited by an electric stimulus applied to a mixed nerve, that is, conduction of the afferent volley to the primary somatosensory cortex. On the other hand, transcranial magnetic stimulation (TMS) of the motor cortex produces MEPs, which are generated by excitation of cortical motoneurons and mediated via corticospinal pathways. When TMS is performed during voluntary muscle contraction, the MEP is followed by a transient pause in electromyographic activity (silent period, SP). Both spinal and intracortical inhibitory mechanisms contribute to the SP. In this study, a total of twenty-two patients were examined and forty-two healthy controls were also studied for comparative purposes. Comparisons were made between patients and healthy controls. Most importantly, statistical tests were made within the group of patients, that is, examining data between affected and non-affected sides and between ON (L-dopa) phase and OFF phase. In patients, no significant changes could be found in all latencies of respective median nerve SEP components, which indicate that the transmission of somatosensory pathway is not involved. However, the amplitude of N30 on the non-affected side was significantly increased at the ON phase. Because the generator of N30 was supposed to be the supplementary motor area (SMA), it has been suggested that N30 is a marker of the functionality of a cortico-subcortico-cortical loop that includes the basal ganglia as well as the premotor area and SMA. Enhanced effects on N30 amplitude were seen on the non-affected side at ON phase indicating that L-dopa facilitates the response of SMA. On the other hand, no change of N30 amplitude on the affected side indicates that the previously mentioned loop was dopamine unresponsive probably due to a defective function of neural structures involved in the SMA-BG-thalamic circuitry. As for the MEP study, a physiologically higher TMS threshold (T) was shown in the dominant hand of normal controls, but the PD patients had the same threshold on both sides of the body. Normal MEP latencies in PD patients indicates that patient's pyramidal motor tract conduction was normal, however, larger MEP amplitudes shown in PD patients indicates that their cortical excitability is higher than that of normal controls. Besides, during OFF phase, the SP of 100%T was shortened on the affected side of PD patients, which coincided with the previously mentioned suggestion that PD patients had higher cortical excitation probably owing to decreased cortical inhibition. However, the shortened SP in PD patients could recover in the ON phase. In conclusion, the results in this study showed that dopaminergic nigrostriatal dysfunction could affect sensorimotor integration, which could be evaluated by using the useful indicators of N30 and SP.
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Chevrier, Éliane. "La perception du contraste de 1er et de 2e ordre chez des personnes atteintes de la maladie de Parkinson sous médication dopaminergique." Thèse, 2007. http://hdl.handle.net/1866/6340.

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Books on the topic "Dopaminergic dysfunction"

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Fuentealba-Evans, José Antonio, and Pablo Henny, eds. Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2799-0.

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Fuentealba-Evans, José Antonio, and Pablo Henny. Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer, 2023.

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BAX, Godfrey. Viagra: Understand Science of Erectile Dysfunction, Modification of Dopaminergic Pathways and Role of Viagra. Independently Published, 2022.

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McCray, Minh A. VIAGRA TABLET: Understanding Science of Erectile Dysfunction, Modification of Dopaminergic Pathways and Role of Viagra in Making and Sustaining Hard Erection. Lulu Press, Inc., 2023.

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Knight, Janice. Viagra Peerless Sex: The Complete Guide on Understanding Erectile Dysfunction Science, Dopaminergic Pathways Modification and the Role of Viagra Pills for Sex. Independently Published, 2022.

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Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.
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Kaar, Stephen J., Steven Potkin, and Oliver Howes. The neurobiology of antipsychotic treatment response and resistance. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0005.

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Dopamine D2/3 receptor occupancy by antipsychotic drugs is central to clinical response and many of their side effects. Yet the locus of dopaminergic alterations in the majority of patients with schizophrenia is not the D2/3 receptor but, instead, presynaptic, comprising elevated striatal dopamine synthesis and release capacity. However, whilst this explains why dopamine D2/3 receptor blockade is effective in many patients, a proportion of patients does not respond. In some this is because of inadequate antipsychotic blockade of dopamine receptors, but there are others who do not respond to antipsychotic treatment despite substantial dopamine D2/3 receptor blockade. The neurobiology of treatment resistance does not seem to involve the presynaptic dopamine dysfunction typically seen in patients, suggesting that it needs different treatments. Disruptions to the glutamatergic system, and to dopamine D1 and D2/3 receptors and serotonin 2A receptors have all been proposed as potential mechanisms underlying treatment resistance and as targets for novel treatments.
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Mahon, Katie, Manuela Russo, and M. Mercedes Perez-Rodriguez. Cognitive Enhancement in Bipolar Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190214401.003.0011.

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Neurocognitive deficits are acknowledged as integral features of bipolar disorder (BD) and are known to contribute to the compromised level of functioning in individuals with BD. This chapter provides an overview of the current state of cognitive enhancement in BD. Few pharmacological agents have been investigated with regard to their potential for pro-cognitive effects in BD. Dopaminergic agents (pramipexole) and stimulants (modafinil, armodafinil, and amphetamine) as adjunctive treatment in BD appear to be promising cognitive enhancers, and there are few ongoing randomized clinical trials targeting both cognitive dysfunctions and clinical symptomatology in BD. Glutamatergic agents (d-cycloserine) may hold promise as potential cognitive enhancing agents in BD; however, as for dopaminergic agents and stimulants, no conclusive data exist. Larger samples and longer follow-up are needed to obtain a deep understanding of the efficacy and safety of these compounds and their role in the neurobiological mechanisms underpinning cognition in BD.
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Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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Book chapters on the topic "Dopaminergic dysfunction"

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Doig, Natalie, and Max Larsson. "Ultrastructural Study of Dopaminergic Axon Terminals." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_1.

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Naneix, Fabien, and Etienne Coutureau. "Dopaminergic Control of Actions and Habits." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_14.

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Stern, Yaakov, and Richard Mayeux. "Possible Dopaminergic Basis for Perceptual Motor Dysfunction." In Advances in Behavioral Biology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2179-8_24.

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Heider, I., V. Lehmensiek, Th Lenk, Th Müller, and A. Storch. "Dopaminergic neurotoxicity of homocysteine and its derivatives in primary mesencephalic cultures." In Focus on Extrapyramidal Dysfunction. Springer Vienna, 2004. http://dx.doi.org/10.1007/978-3-7091-0579-5_1.

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Reynolds, Lauren M., Andrea Harée Pantoja-Urbán, Del MacGowan, Colleen Manitt, Dominique Nouel, and Cecilia Flores. "Quantifying Dopaminergic Innervation in Rodents Using Unbiased Stereology." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_2.

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Pautassi, Ricardo M., Aranza Wille-Bille, Macarena S. Fernández, and María Carolina Fabio. "Ethanol Intake on Preclinical Models: Methods of Assessment and Effects on Dopamine Signaling." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_8.

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Perez-Valenzuela, Enzo, and Steven R. Laviolette. "Preclinical Models of THC and Nicotine Exposure During Adolescent Brain Development: Modeling Neuropsychiatric Phenotypes Related to Dopaminergic Transmission." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_9.

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Garcia-Nuñez, Ximena Paz, Carolina Astudillo-Valenzuela, and Romulo Fuentes-Flores. "Multi-circuit Recording in Animal Models of Parkinson's Disease." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_12.

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Clark, Philip J., and Rodrigo A. España. "Fast Scan Cyclic Voltammetry to Assess Dopamine Function: From Circuits to Behavior." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_11.

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Parr, Ashley, Bart Larsen, Finnegan Calabro, Brenden Tervo-Clemmens, and Beatriz Luna. "Neuroimaging Human Dopamine-Related Neurophysiology Across Development." In Dopaminergic System Function and Dysfunction: Experimental Approaches. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2799-0_13.

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Conference papers on the topic "Dopaminergic dysfunction"

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Pinheiro, Amanda Pereira Sindeaux, Pedro Vitor Ferreira Rodrigues, Raoni de Oliveira da Silva Domingues, and Leonardo José Rodrigues Araújo Melo. "Gastrointestinal dysmotility associated with Parkinson’s disease’s mechanism." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.461.

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Introduction: Parkinson’s Disease (PD) is a condition of the brain that consiste of the death of dopaminergic neurons in the substantia nigra, therefore causing dyskinesias and dystonias. Besides the motor symptoms, the neurogastro motility is affected by the disease, since gastrointestinal dysfunction is a frequent and clinically relevant symptom of PD. Objectives: To link the neural pathways and neurotransmitters that involve the neuroenteric system control and the PD’s pathology. Methods: A systematic literature review was performed based on data extraction through the advanced research engine from Pubmed. Publications with the descriptors “dysmotility” OR “gastro motility” AND “Parkinson” were selected. Results: Through clinical and pre-clinical studies on PD, there has been hypothesized a gut-brain axis that is connected through hormones, neurotransmitters and dopamanergic inputs. This hypothesis is supported by evidence in the showing of accumulation of alpha-synuclein in the vagal system and Enteric Nervous System, the use of drugs such as peripheral dopaminergic blockers and serotonin for gastroparesis, the ghrelin effects on the central dopaminergic system through modulation of the mesencephalic dopaminergic signaling tested on rats, the gastrointestinal autonomic neuropathy detected in PD patients and the establishment of gut dysmotility before motor onset symptoms. Therefore, dysmotility isues such as delayed gastric emptying may not only be a symptom of PD, but also contrubute to the pathogenesis itself through impaired signaling. Conclusion: The gut-brain axis can be not only a tool for PD diagnosis but also a treatment target to restrain the advance of the disease. Although many articles are related this subject, there is a lack of designed trials for atypical movement disorders. To explore the dysmotility in PD, there is a need for multi-modality standardized tests to evaluate severity and prevalence.
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Dakhel, Sami, Jonathan Elias, and Alexander King. "Analyzing the Effectiveness of Transcutaneous Auricular Vagus Nerve Stimulation on Parkinson’s Disease Related Gait Function: A Systematic Review and Meta-Analysis." In 28th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2024. https://doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.213_2024.

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Background: Those suffering from Parkinson’s Disease often experience a shuffling gait, alongside many other symptoms, due to the degradation of dopaminergic neurons in the substantia nigra. Transcutaneous auricular vagus nerve stimulation (taVNS) operates by non-invasively applying an electrical current to the cutaneous receptive field formed by the auricular branch of the vagus nerve in the outer ear. We sought to determine if taVNS would serve as a non-invasive alternative to addressing Parkinson’s related gait dysfunction. Purpose: This systematic review and meta-analysis analyzes the effectiveness of taVNS on the reduction of gait dysfunction caused by Parkinson’s Disease. Methods: The systematic review and meta-analysis followed the 2020 PRISMA guidelines. Five online databases were screened (Embase, Cochrane, Web Of Science, Scopus, PubMed) for studies that included pre-treatment and post-treatment data of the Unified Parkinson’s Disease Rating Scale (UPDRS), gait speed, sway length, and stride length. After our screening process, 2 double-blinded randomized controlled trials (RCTs) were included in the analysis. The meta-analysis was conducted using SPSS. Results: After treatment with taVNS, there was a low, but clinically significant increase in walk speed (Cohen’s d = 0.34) and in stride length (Cohen’s d = 0.20). All other variables did not yield significant changes. Conclusion: Our results suggest that taVNS is only partially effective in improving gait dysfunction related to Parkinson’s Disease, with slight increases in walk speed and stride length. However, with a sample size of only 20 patients, future RCTs with larger sample sizes are needed in order to truly solidify the yielded results. Additionally, further RCTs examining taVNS on gait dysfunction with a placebo group compared to an experimental group would be beneficial in analyzing the effectiveness of such a treatment modality.
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Ghosh, Dipannita, Md Ashiqur Rahman, Ali Ashraf, and Nazmul Islam. "Graphene-Conductive Polymer-Based Electrochemical Sensor for Dopamine Detection." In ASME 2022 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/imece2022-96193.

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Abstract The central nervous system’s (CNS) dopaminergic system dysfunction has been linked to neurological illnesses like schizophrenia and Parkinson’s disease. As a result, sensitive and selective detection of dopamine is critical for the early diagnosis of illnesses associated with aberrant dopamine levels. In this research, we have investigated the performance of electrochemical screen-printed sensors for different concentrations of dopamine detection using graphene-based conductive PEDOT: PSS(G-PEDOT: PSS) and Polyaniline(G-PANI) inks on the working electrode and compared the sensitivity. SEM characterization technique has been performed to visualize the microstructures of the proposed inks. We have investigated cyclic voltammetry (CV) electrochemical techniques with ferri/ferrocyanide redox couple to assess the efficiency of the designed electrodes in detecting dopamine. G-PANI ink has shown to have better LOD and stability to detect dopamine with screen-printed electrodes. Further, we have also studied electrochemical analysis for the selective detection of dopamine without the interference of Ascorbic Acid (AA).
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Oliveira, Arthu Línniker Lopes de, Gilciane Bezerra Alves dos Santos, Camila Raposo Fônseca, and Igor Thiago Borges de Queiroz e. Siva. "Paradoxical neuroplasticity due to post-Covid-19 astrocytosis in children and adolescents." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.384.

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Background: According to the American Academy of Pediatrics, there are approximately 3.28 millions of SARS-CoV-2 infections among children and adolescents as of March 2021. A modulation of the synaptic environment has been described due to astrocytosis caused by SARS-CoV-2 along with a decrease in cognitive stimuli aggravated by social isolation. Objectives: To correlate the slowness of brain connectivity with astrocytosis caused by SARS-CoV-2 in the pediatric population in post-Covid-19. Methods: Literary review carried out at PubMed from January to April 2021, using “Brain infection”, “SARS-CoV-2”, “Children’’, and “Astrocytosis” as descriptors. It was selected 183 articles in english published in the last 5 years, of which only 10 were closer to the research subject. Results: SARS-CoV-2 led by the Spike protein of the virus causes remodeling in glucose metabolism, causing deviation in the consumption of lactate (metabolic substrate of astrocytes), compensatorily way to neuronal malnutrition. To supply their metabolism, astrocytes are taken to a glutamate consumption responsible for synaptic plasticity due to dopamine synthesis (DA). Furthermore, astrocytosis stimulates apoptosis of SH-SY5Y cells, which are linked to dopaminergic expression in synaptic clefts, further accentuating the decline in DA levels. Conclusions: Cortical dysfunctions resulting from neural malnutrition and low cognitive stimulation during social isolation favor an intense neuroplastic paradox in the pediatric population during the critical period.
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Rodrigues, Amanda Gabriele Coelho, Ana Cassia Gonzalez dos Santos Estrela, Ligia Aurelio Vieira Pianta Tavares, and Beatriz Trajano Costa da Silva. "Hypopituitarism versus spontaneous subarachnoid hemorrhage." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.379.

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Introduction: Spontaneous subarachnoid hemorrhage (SAH) is a medical emergency characterized by bleeding in the subarachnoid space, of nontraumatic etiology. Studies demonstrate the relationship of HSA in the pathogenesis of hypopituitarism, which are important due to the need to develop new therapeutic and diagnostic tools. Objectives: To highlight hormonal complications after SAH. Methods: A literature review was carried out in the Scielo and PubMed databases, using the descriptors: “aneurysmal subarachnoid haemorrhage” “hormone deficiency” and “hypopituitarism”, limited to articles in English, available in full and published in the last five years. Twenty-seven articles were found, of which eight entered the study. Results: The study indicates that hypopituitarism after SAH is associated with an unfavorable neurological outcome. Pointing to changes in gonadotropins in men, with less hair on the face and body, gynecomastia and hypogonadism. Anemia due to decreased erythropoiesis associated with hypogonadism, growth hormone deficiency associated with decreased exercise tolerance, increased centripetal fat, and premature atherosclerosis. Hyperprolactinemia is common in this group of patients due to interference with dopaminergic inhibition. These hormonal dysfunctions trigger fatigue, headache, mood swings, depression, cognitive impairment and inability to perform daily activities in these patients, often being confused with neurological sequelae resulting from the patient’s cerebral hemorrhage. Conclusion: The endocrinological control of patients with SAH is relevant, due to its uncertain immediate prognosis. Hypopituitarism is a relevant complication, which if identified early on, there is the possibility of hormone replacement and improvements in the patient’s quality of life. Knowledge about the complications of SAH has the role of clarifying not only hypopituitarism, but also cognitive diseases, contributing to elucidate possible therapeutic targets, gaps to be investigated on the subject.
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Reports on the topic "Dopaminergic dysfunction"

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Surmeier, D. J. Calcium Homeostatasis and Mitochondrial Dysfunction in Dopaminergic Neurons of the Substantia Nigra. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada519458.

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Zhang, Yu, Chaoliang Sun, Hengxi Xu, et al. Connectivity-Based Subtyping of De Novo Parkinson Disease: Biomarkers, Medication Effects and Longitudinal Progression. Progress in Neurobiology, 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.04.

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Parkinson's disease (PD) is characterized by divergent clinical symptoms and prognosis, suggesting the presence of distinct subtypes. Identifying these subtypes is crucial for understanding the underlying pathophysiology, predicting disease progression, and developing personalized treatments. In this study, we propose a connectivity-based subtyping approach, which measures each patient's deviation from the reference structural covariance networks established in healthy controls. Using data from the Parkinson's Progression Markers Initiative, we identified two distinct subtypes of de novo PD patients: 248 patients with typical cortical-striato-thalamic dysfunctions and 41 patients showing weakened dorsal raphe nucleus (DRN)-to-cortical/striatal projections. The proposed subtyping approach demonstrated high stability in terms of random sampling of healthy or diseased population and longitudinal prediction at follow-up visits, outperforming the traditional motor phenotypes. Compared to the typical PD, patients with the DRN-predominant subtype were characterized by less server motor symptoms at baseline and distinct imaging biomarkers, including larger striatal volumes, higher concentration of cerebrospinal fluid amyloid-β and amyloid-β/t(p)-tau ratio. Subtype-specific associations and drug effects were identified that the DRN subtype exhibited more pronounced medication effects on motor symptoms, potentially regulated by DRN serotonergic modulation through striatal dopaminergic neurons. The DRN serotonergic inputs also regulated non-motor symptoms, the aggregation of CSF biomarkers and the conversion to more severe disease states. Our findings suggest that the DRN-predominant subtype represents a unique clinical and biological phenotype of PD characterized by an enhanced response to anti-parkinsonian treatment, more favorable prognosis and slower progression of dopamine depletion. This study may contribute to clinical practice of precision medicine, early invention and individualized treatments in PD and other neurodegenerative diseases.
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