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Journal articles on the topic 'Dopaminergic dysfunction'

Author: Grafiati

Published: 7 June 2025

Last updated: 17 July 2025

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1

&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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2

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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3

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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4

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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5

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

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6

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 relev

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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

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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-synuclei

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9

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 blu

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10

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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11

Vaccari, A., Z. L. Rossetti, G. de Montis, E. Stefanini, E. Martino, and G. L. Gessa. "Neonatal hypothyroidism induces striatal dopaminergic dysfunction." Neuroscience 35, no. 3 (1990): 699–706. http://dx.doi.org/10.1016/0306-4522(90)90340-a.

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12

Steeves, Thomas D. L., Ji Hyun Ko, David M. Kideckel, et al. "Extrastriatal dopaminergic dysfunction in tourette syndrome." Annals of Neurology 67, no. 2 (2010): 170–81. http://dx.doi.org/10.1002/ana.21809.

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13

Wichmann, Thomas. "Commentary: Dopaminergic dysfunction in DYT1 dystonia." Experimental Neurology 212, no. 2 (2008): 242–46. http://dx.doi.org/10.1016/j.expneurol.2008.04.020.

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14

Uc, Ergun Y., Jon Tippin, Kelvin L. Chou, Bradley A. Erickson, Kevin C. Doerschug, and Decontee M. Jimmeh Fletcher. "Non-motor Symptoms in Parkinson’s Disease." US Neurology 07, no. 02 (2011): 113. http://dx.doi.org/10.17925/usn.2011.07.02.113.

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In addition to typical motor dysfunction (parkinsonism), diverse non-motor symptoms (NMS) are frequently observed in patients with Parkinsons disease (PD). Some NMS may antedate the diagnosis of PD. Examples of NMS include cognitive impairment, autonomic dysfunction, visual dysfunction, sleep abnormalities, and psychiatric disorders. NMS are associated with wide-ranging abnormalities in extranigral dopaminergic systems and non-dopaminergic (e.g. cholinergic, noradrenergic, serotoninergic) systems. The type and severity of NMS vary based on age, disease severity, and predominant motor symptoms

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Uc, Ergun Y., Jon Tippin, Kelvin L. Chou, Bradley A. Erickson, Kevin C. Doerschug, and Decontee M. Jimmeh Fletcher. "Non-motor Symptoms in Parkinson’s Disease." European Neurological Review 7, no. 1 (2012): 35. http://dx.doi.org/10.17925/enr.2012.07.01.35.

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In addition to typical motor dysfunction (parkinsonism), diverse non-motor symptoms (NMS) are frequently observed in patients with Parkinson’s disease (PD). Some NMS may antedate the diagnosis of PD. Examples of NMS include cognitive impairment, autonomic dysfunction, visual dysfunction, sleep abnormalities and psychiatric disorders. NMS are associated with wide-ranging abnormalities in extranigral dopaminergic systems and non-dopaminergic (e.g. cholinergic, noradrenergic, serotoninergic) systems. The type and severity of NMS vary based on age, disease severity and predominant motor symptoms.

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16

Goiran, Thomas, Mohamed A. Eldeeb, Cornelia E. Zorca, and Edward A. Fon. "Hallmarks and Molecular Tools for the Study of Mitophagy in Parkinson’s Disease." Cells 11, no. 13 (2022): 2097. http://dx.doi.org/10.3390/cells11132097.

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The best-known hallmarks of Parkinson’s disease (PD) are the motor deficits that result from the degeneration of dopaminergic neurons in the substantia nigra. Dopaminergic neurons are thought to be particularly susceptible to mitochondrial dysfunction. As such, for their survival, they rely on the elaborate quality control mechanisms that have evolved in mammalian cells to monitor mitochondrial function and eliminate dysfunctional mitochondria. Mitophagy is a specialized type of autophagy that mediates the selective removal of damaged mitochondria from cells, with the net effect of dampening t

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Bronner, Gila, and David B. Vodušek. "Management of sexual dysfunction in Parkinson’s disease." Therapeutic Advances in Neurological Disorders 4, no. 6 (2011): 375–83. http://dx.doi.org/10.1177/1756285611411504.

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Nonmotor symptoms, among them sexual dysfunction, are common and underrecognized in patients with Parkinson disease; they play a major role in the deterioration of quality of life of patients and their partners. Loss of desire and dissatisfaction with their sexual life is encountered in both genders. Hypersexuality (HS), erectile dysfunction and problems with ejaculation are found in male patients, and loss of lubrication and involuntary urination during sex are found in female patients. Tremor, hypomimia, muscle rigidity, bradykinesia, ‘clumsiness’ in fine motor control, dyskinesias, hypersal

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18

Schrantee, Anouk, Lena Václavů, Dennis F. R. Heijtel, et al. "Dopaminergic System Dysfunction in Recreational Dexamphetamine Users." Neuropsychopharmacology 40, no. 5 (2014): 1172–80. http://dx.doi.org/10.1038/npp.2014.301.

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19

Butterworth, Roger F., Laurent Spahr, Suzanne Fontaine, and Gilles Pomier Layrargues. "Manganese toxicity, dopaminergic dysfunction and hepatic encephalopathy." Metabolic Brain Disease 10, no. 4 (1995): 259–67. http://dx.doi.org/10.1007/bf02109357.

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20

Heinz, A., and F. Schlagenhauf. "Dopaminergic Dysfunction in Schizophrenia: Salience Attribution Revisited." Schizophrenia Bulletin 36, no. 3 (2010): 472–85. http://dx.doi.org/10.1093/schbul/sbq031.

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21

Liss, Birgit, and Jochen Roeper. "ATP-Sensitive Potassium Channels in Dopaminergic Neurons: Transducers of Mitochondrial Dysfunction." Physiology 16, no. 5 (2001): 214–17. http://dx.doi.org/10.1152/physiologyonline.2001.16.5.214.

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ATP-sensitive potassium (KATP) channels directly couple the metabolic state of a cell to its electrical activity. Dopaminergic midbrain neurons express alternative types of KATP channels mediating their differential response to mitochondrial complex I inhibition. Because reduced complex I activity is present in Parkinson's Disease, differential KATP channel expression suggests a novel candidate mechanism for selective dopaminergic degeneration.

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22

Heinz, A. "Dopaminergic dysfunction in alcoholism and schizophrenia – psychopathological and behavioral correlates." European Psychiatry 17, no. 1 (2002): 9–16. http://dx.doi.org/10.1016/s0924-9338(02)00628-4.

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SummaryDysfunction of central dopaminergic neurotransmission has been implicated in the pathogenesis of schizophrenia as well as drug and alcohol dependence. Different drugs of abuse stimulate dopamine release in the ventral striatum and thus reinforce drug consumption. Increased subcortical dopamine release has also been associated with the pathogenesis of positive symptoms in schizophrenia and may be driven by a prefrontal dopaminergic dysfunction. These seemingly heterogeneous findings may be explained by recent research in non-human primates. According to these studies, reward anticipation

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23

Jovanovic, Predrag, Yidan Wang, Jean-Philippe Vit, et al. "Sustained chemogenetic activation of locus coeruleus norepinephrine neurons promotes dopaminergic neuron survival in synucleinopathy." PLOS ONE 17, no. 3 (2022): e0263074. http://dx.doi.org/10.1371/journal.pone.0263074.

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Dopaminergic neuron degeneration in the midbrain plays a pivotal role in motor symptoms associated with Parkinson’s disease. However, non-motor symptoms of Parkinson’s disease and post-mortem histopathology confirm dysfunction in other brain areas, including the locus coeruleus and its associated neurotransmitter norepinephrine. Here, we investigate the role of central norepinephrine-producing neurons in Parkinson’s disease by chronically stimulating catecholaminergic neurons in the locus coeruleus using chemogenetic manipulation. We show that norepinephrine neurons send complex axonal project

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24

Guatteo, Ezia, Nicola Berretta, Vincenzo Monda, Ada Ledonne, and Nicola Biagio Mercuri. "Pathophysiological Features of Nigral Dopaminergic Neurons in Animal Models of Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 9 (2022): 4508. http://dx.doi.org/10.3390/ijms23094508.

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The degeneration of nigral dopaminergic neurons is considered the hallmark of Parkinson’s disease (PD), and it is triggered by different factors, including mitochondrial dysfunction, Lewy body accumulation, neuroinflammation, excitotoxicity and metal accumulation. Despite the extensive literature devoted to unravelling the signalling pathways involved in neuronal degeneration, little is known about the functional impairments occurring in these cells during illness progression. Of course, it is not possible to obtain direct information on the properties of the dopaminergic cells in patients. Ho

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25

Schlagenhauf, F., G. Juckel, and A. Heinz. "Relationships between negative symptoms and abnormalities in the anticipatory component of reward." European Psychiatry 26, S2 (2011): 2070. http://dx.doi.org/10.1016/s0924-9338(11)73773-7.

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A dysfunction of the dopaminergic reward system has been postulated in the pathophysiology of schizophrenia. A subcortical hyperdopaminergic state in unmedicated schizophrenia patients has been associated with the pathogenesis of positive symptoms and a prefrontal hypodopaminergic state with cognitive and negative symptoms. But negative symptoms like anhedonia have also been hypothesized to be associated with a dysfunction of the mesolimbic dopaminergic system. However, preclinical studies indicate that the mesolimbic dopaminergic system mediates motivation and incentive salience of reward-ind

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26

Vorhees, Nathaniel W., Samantha L. Groenwold, Mackenzie T. Williams, et al. "Olfactory Dysfunction in a Novel Model of Prodromal Parkinson’s Disease in Adult Zebrafish." International Journal of Molecular Sciences 26, no. 10 (2025): 4474. https://doi.org/10.3390/ijms26104474.

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Olfactory dysfunction is a clinical marker of prodromal Parkinson’s disease (PD), yet the underlying mechanisms remain unclear. To explore this relationship, we developed a zebrafish model that recapitulates the olfactory impairment observed in prodromal PD without affecting motor function. We used zebrafish due to their olfactory system’s similarity to mammals and their unique nervous system regenerative capacity. By injecting 6-hydroxydopamine (6-OHDA) into the dorsal telencephalic ventricle, we observed a significant loss of dopaminergic (DA) periglomerular neurons in the olfactory bulb (OB

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Blanco-Hernán, Pedro, Lorena Aguado, María José Asensio, et al. "The Retinal Dopaminergic Circuit as a Biomarker for Huntington’s and Alzheimer’s Diseases." International Journal of Molecular Sciences 26, no. 12 (2025): 5532. https://doi.org/10.3390/ijms26125532.

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Retinal dysfunction is emerging as a potential early marker of neurodegenerative diseases. Within the retina, the dopaminergic circuit, comprising dopaminergic amacrine cells, dopamine synthesis and turnover, and dopamine receptor signalling, is essential for visual processing, particularly colour contrast perception. Disruption of this circuit may underline early retinal alterations observed in Huntington’s disease (HD) and Alzheimer’s disease (AD). In this study, we systematically analysed retinal dopaminergic dysfunction in murine models of HD (genetic origin) and AD (sporadic), across diff

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Huang, Chunhui, Zaijun Zhang, and Wei Cui. "Marine-Derived Natural Compounds for the Treatment of Parkinson’s Disease." Marine Drugs 17, no. 4 (2019): 221. http://dx.doi.org/10.3390/md17040221.

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Parkinson’s disease (PD) is a neurodegenerative disorder caused by the loss of dopaminergic neurons, leading to the motor dysfunctions of patients. Although the etiology of PD is still unclear, the death of dopaminergic neurons during PD progress was revealed to be associated with the abnormal aggregation of α-synuclein, the elevation of oxidative stress, the dysfunction of mitochondrial functions, and the increase of neuroinflammation. However, current anti-PD therapies could only produce symptom-relieving effects, because they could not provide neuroprotective effects, stop or delay the dege

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Kocar, Thomas Derya, Hans-Peter Müller, and Jan Kassubek. "Differential functional connectivity in thalamic and dopaminergic pathways in restless legs syndrome: a meta-analysis." Therapeutic Advances in Neurological Disorders 13 (January 2020): 175628642094167. http://dx.doi.org/10.1177/1756286420941670.

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Objective: Restless legs syndrome (RLS) is a sensorimotor disorder with alterations in somatosensory processing in association with a dysfunctional cerebral network, involving the basal ganglia, limbic network, and sensorimotor pathways. Resting state functional magnetic resonance imaging (MRI) is a powerful tool to provide in vivo insight into functional processing and as such is of special interest in RLS considering the widespread pattern of networks involved in this disorder. In this meta-analysis of resting state functional MRI studies, we analyzed the preponderance of functional connecti

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Zárate, Rafaella V., Sergio Hidalgo, Nicole Navarro, et al. "An Early Disturbance in Serotonergic Neurotransmission Contributes to the Onset of Parkinsonian Phenotypes in Drosophila melanogaster." Cells 11, no. 9 (2022): 1544. http://dx.doi.org/10.3390/cells11091544.

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Parkinson’s disease (PD) is a neurodegenerative disease characterized by motor symptoms and dopaminergic cell loss. A pre-symptomatic phase characterized by non-motor symptoms precedes the onset of motor alterations. Two recent PET studies in human carriers of mutations associated with familial PD demonstrate an early serotonergic commitment—alteration in SERT binding—before any dopaminergic or motor dysfunction, that is, at putative PD pre-symptomatic stages. These findings support the hypothesis that early alterations in the serotonergic system could contribute to the progression of PD, an i

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Rathor, Priya, and Ratnasekhar Ch. "Metabolic Basis of Circadian Dysfunction in Parkinson’s Disease." Biology 12, no. 10 (2023): 1294. http://dx.doi.org/10.3390/biology12101294.

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Parkinson’s disease (PD) is one of the most common neurodegenerative disorders. The management of PD is a challenging aspect for general physicians and neurologists. It is characterized by the progressive loss of dopaminergic neurons. Impaired α-synuclein secretion and dopamine release may cause mitochondrial dysfunction and perturb energy metabolism, subsequently altering the activity and survival of dopaminergic neurons, thus perpetuating the neurodegenerative process in PD. While the etiology of PD remains multifactorial, emerging research indicates a crucial role of circadian dysfunction i

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Vyas, Nora S., Neva H. Patel, Kuldip S. Nijran, Adil Al-Nahhas, and Basant K. Puri. "Insights into schizophrenia using positron emission tomography: building the evidence and refining the focus." British Journal of Psychiatry 197, no. 1 (2010): 3–4. http://dx.doi.org/10.1192/bjp.bp.109.073882.

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SummarySchizophrenia involves dysregulation in dopaminergic transmission. Studies show heightened presynaptic striatal dopaminergic function and elevated striatal D2/D3 receptor density in the brain. Cognitive impairments result from hypostimulation of D1 receptors and are associated with dysfunction in the prefrontal cortex. Here we discuss relevant positron emissions tomography (PET) studies and provide future directions.

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Nguyen, Maria, and Dimitri Krainc. "LRRK2 phosphorylation of auxilin mediates synaptic defects in dopaminergic neurons from patients with Parkinson’s disease." Proceedings of the National Academy of Sciences 115, no. 21 (2018): 5576–81. http://dx.doi.org/10.1073/pnas.1717590115.

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Recently identified Parkinson’s disease (PD) genes involved in synaptic vesicle endocytosis, such as DNAJC6 (auxilin), have further implicated synaptic dysfunction in PD pathogenesis. However, how synaptic dysfunction contributes to the vulnerability of human dopaminergic neurons has not been previously explored. Here, we demonstrate that commonly mutated, PD-linked leucine-rich repeat kinase 2 (LRRK2) mediates the phosphorylation of auxilin in its clathrin-binding domain at Ser627. Kinase activity-dependent LRRK2 phosphorylation of auxilin led to differential clathrin binding, resulting in di

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34

Vasile, Titus Mihai, and Ovidiu Bajenaru. "Dopaminergic and non-dopaminergic mechanisms of non-motor symptoms of Parkinson disease." Romanian Journal of Neurology 11, no. 4 (2012): 158–64. http://dx.doi.org/10.37897/rjn.2012.4.2.

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During the last years, the non-motor aspects of Parkinson’s disease were in the focus of the attention in Movement Disorders Society and experts. Some clinical and research instruments like NMSS (Non-Motor Symptoms Scale) help clinicians to recognize and evaluate these aspects that are common and occur across all stages of PD. Some non-motor symptoms like sleep problems, autonomic dysfunction and pain are partly dopaminergic but others are non-dopaminergic. When they are treatable, the treatment can increase the quality of life for these patients.

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von Stockum, Sophia, Alvaro Sanchez-Martinez, Samantha Corrà, et al. "Inhibition of the deubiquitinase USP8 corrects a Drosophila PINK1 model of mitochondria dysfunction." Life Science Alliance 2, no. 2 (2019): e201900392. http://dx.doi.org/10.26508/lsa.201900392.

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Aberrant mitochondrial dynamics disrupts mitochondrial function and contributes to disease conditions. A targeted RNA interference screen for deubiquitinating enzymes (DUBs) affecting protein levels of multifunctional mitochondrial fusion protein Mitofusin (MFN) identified USP8 prominently influencing MFN levels. Genetic and pharmacological inhibition of USP8 normalized the elevated MFN protein levels observed in PINK1 and Parkin-deficient models. This correlated with improved mitochondrial function, locomotor performance and life span, and prevented dopaminergic neurons loss in Drosophila PIN

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36

Simonsen, Ulf, Simon Comerma-Steffensen, and Karl-Erik Andersson. "Modulation of Dopaminergic Pathways to Treat Erectile Dysfunction." Basic & Clinical Pharmacology & Toxicology 119 (October 2016): 63–74. http://dx.doi.org/10.1111/bcpt.12653.

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Marek, Kenneth. "Dopaminergic Dysfunction in Parkinsonism: New Lessons from Imaging." Neuroscientist 5, no. 5 (1999): 333–40. http://dx.doi.org/10.1177/107385849900500519.

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38

Hunter, P. C., J. Crameri, S. Austin, M. C. Woodward, and A. J. Hughes. "Response of parkinsonian swallowing dysfunction to dopaminergic stimulation." Journal of Neurology, Neurosurgery & Psychiatry 63, no. 5 (1997): 579–83. http://dx.doi.org/10.1136/jnnp.63.5.579.

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39

Jiang, Chuantao, Xinhua Wan, Yi He, Tianhong Pan, Joseph Jankovic, and Weidong Le. "Age-dependent dopaminergic dysfunction in Nurr1 knockout mice." Experimental Neurology 191, no. 1 (2005): 154–62. http://dx.doi.org/10.1016/j.expneurol.2004.08.035.

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Riesco, Marta F., David G. Valcarce, Juan Manuel Martínez-Vázquez, et al. "Male reproductive dysfunction in Solea senegalensis: new insights into an unsolved question." Reproduction, Fertility and Development 31, no. 6 (2019): 1104. http://dx.doi.org/10.1071/rd18453.

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Senegalese sole (Solea senegalensis) is a species with a high commercial value that exhibits a reproductive dysfunction in males born and raised in captivity (F1) that hinders their sustainable culture. The present study evaluates the sperm quality and dopaminergic pathway of males born in the wild environment and of F1 males. Traditional sperm analyses were performed, finding only significant differences in curvilinear velocity (VCL) and no significant differences in viability and total motility. No differences in global sperm methylation were observed either in spermatozoa or brain between t

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Jauhar, S., M. Veronese, M. Rogdaki, et al. "Regulation of dopaminergic function: an [18F]-DOPA PET apomorphine challenge study in humans." Translational Psychiatry 7, no. 2 (2017): e1027-e1027. http://dx.doi.org/10.1038/tp.2016.270.

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Abstract Dopaminergic function has a key role in normal brain function, dopaminergic dysfunction being implicated in numerous neuropsychiatric disorders. Animal studies show that dopaminergic stimulation regulates dopaminergic function, but it is not known whether this exists in humans. In the first study (study 1), we measured dopamine synthesis capacity (indexed as K i cer) to identify the relationship between baseline and change in K i cer under resting conditions for comparison with effects of dopaminergic stimulation. In the second study (study 2), we used a within-subjects design to test

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Malapani, Chara, Bernard Deweer, and John Gibbon. "Separating Storage from Retrieval Dysfunction of Temporal Memory in Parkinson's Disease." Journal of Cognitive Neuroscience 14, no. 2 (2002): 311–22. http://dx.doi.org/10.1162/089892902317236920.

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Dysfunction of the basal ganglia and the brain nuclei interconnected with them leads to disturbances of movement and cognition exemplified in Parkinson's disease (PD) and Huntington's disease, including disordered timing of movements and impaired time estimation. Previous research has shown that whereas striatal damage in animals can result in the loss of temporal control over behavior, dopaminergic deregulation in the human striatum associated with PD distorts the memory for time. Here we show a dissociation between deficits in storage (writing to) and retrieval (reading from) temporal memory

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Phung, Viet-Duc, Won-Sik Jung, Thuy-An Nguyen, Jong-Hoon Kim, and Sang-Wha Lee. "Reliable and quantitative SERS detection of dopamine levels in human blood plasma using a plasmonic Au/Ag nanocluster substrate." Nanoscale 10, no. 47 (2018): 22493–503. http://dx.doi.org/10.1039/c8nr06444j.

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Greenamyre, J. Timothy, Gillian MacKenzie, Tsung-I. Peng, and Stacy E. Stephans. "Mitochondrial dysfunction in Parkinson's disease." Biochemical Society Symposia 66 (September 1, 1999): 85–97. http://dx.doi.org/10.1042/bss0660085.

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The cause of Parkinson's disease (PD) is unknown, but reduced activity of complex I of the electron-transport chain has been implicated in the pathogenesis of both mitochondrial permeability transition pore-induced Parkinsonism and idiopathic PD. We developed a novel model of PD in which chronic, systemic infusion of rotenone, a complex-I inhibitor, selectively kills dopaminergic nerve terminals and causes retrograde degeneration of substantia nigra neurons over a period of months. The distribution of dopaminergic pathology replicates that seen in PD, and the slow time course of neurodegenerat

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45

Houlihan, David J. "Psychostimulant treatment of combat-related posttraumatic stress disorder." Journal of Psychopharmacology 25, no. 11 (2010): 1568–72. http://dx.doi.org/10.1177/0269881110385600.

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The objective of this paper is to describe three cases of combat-related posttraumatic stress disorder (PTSD), largely refractory to standard medication treatment who responded well to psychostimulant treatment. Symptoms of PTSD potentially result from chronic, stress-induced dopaminergic dysfunction in the prefrontal cortex/basal ganglia system. Psychostimulants, by their relative propensity to enhance dopamine (DA) activity within these brain regions, may have particular value in targeting this dysfunction. Evidence of dopaminergic dysfunction following chronic stress is reviewed and possibl

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46

Imai, Yuzuru. "Editorial for the Special Issue “Animal Models of Parkinson’s Disease and Related Disorders”." International Journal of Molecular Sciences 21, no. 12 (2020): 4250. http://dx.doi.org/10.3390/ijms21124250.

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Pasquini, Jacopo, Rory Durcan, Louise Wiblin, et al. "Clinical implications of early caudate dysfunction in Parkinson’s disease." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 10 (2019): 1098–104. http://dx.doi.org/10.1136/jnnp-2018-320157.

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ObjectiveAlthough not typical of Parkinson’s disease (PD), caudate dopaminergic dysfunction can occur in early stages of the disease. However, its frequency and longitudinal implications in large cohorts of recently diagnosed patients remain to be established. We investigated the occurrence of caudate dopaminergic dysfunction in the very early phases of PD (<2 years from diagnosis) using 123I-FP-CIT single photon emission CT and determined whether it was associated with the presence or subsequent development of cognitive impairment, depression, sleep and gait problems.MethodsPatients with P

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Rasheed, Naila, and Abdullah Alghasham. "Central Dopaminergic System and Its Implications in Stress-Mediated Neurological Disorders and Gastric Ulcers: Short Review." Advances in Pharmacological Sciences 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/182671.

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For decades, it has been suggested that dysfunction of dopaminergic pathways and their associated modulations in dopamine levels play a major role in the pathogenesis of neurological disorders. Dopaminergic system is involved in the stress response, and the neural mechanisms involved in stress are important for current research, but the recent and past data on the stress response by dopaminergic system have received little attention. Therefore, we have discussed these data on the stress response and propose a role for dopamine in coping with stress. In addition, we have also discussed gastric

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Tomasella, Eugenia, Lucila Bechelli, Mora Belén Ogando, et al. "Deletion of dopamine D2 receptors from parvalbumin interneurons in mouse causes schizophrenia-like phenotypes." Proceedings of the National Academy of Sciences 115, no. 13 (2018): 3476–81. http://dx.doi.org/10.1073/pnas.1719897115.

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Excessive dopamine neurotransmission underlies psychotic episodes as observed in patients with some types of bipolar disorder and schizophrenia. The dopaminergic hypothesis was postulated after the finding that antipsychotics were effective to halt increased dopamine tone. However, there is little evidence for dysfunction within the dopaminergic system itself. Alternatively, it has been proposed that excessive afferent activity onto ventral tegmental area dopaminergic neurons, particularly from the ventral hippocampus, increase dopamine neurotransmission, leading to psychosis. Here, we show th

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Doé de Maindreville, A., S. Bakchine, D. Papathanassiou, P. Orquevaux, C. Tranchant, and E. Roze. "Evidence of presynaptic dopaminergic dysfunction in acute methanol intoxication." Revue Neurologique 173, no. 6 (2017): 420–22. http://dx.doi.org/10.1016/j.neurol.2017.03.014.

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