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1.
The Principle of Nanomaterials Based Surface Plasmon Resonance Biosensors and Its Potential for Dopamine Detection.
Kamal Eddin, FB, Fen, YW
Molecules (Basel, Switzerland). 2020;(12)
Abstract
For a healthy life, the human biological system should work in order. Scheduled lifestyle and lack of nutrients usually lead to fluctuations in the biological entities levels such as neurotransmitters (NTs), proteins, and hormones, which in turns put the human health in risk. Dopamine (DA) is an extremely important catecholamine NT distributed in the central nervous system. Its level in the body controls the function of human metabolism, central nervous, renal, hormonal, and cardiovascular systems. It is closely related to the major domains of human cognition, feeling, and human desires, as well as learning. Several neurological disorders such as schizophrenia and Parkinson's disease are related to the extreme abnormalities in DA levels. Therefore, the development of an accurate, effective, and highly sensitive method for rapid determination of DA concentrations is desired. Up to now, different methods have been reported for DA detection such as electrochemical strategies, high-performance liquid chromatography, colorimetry, and capillary electrophoresis mass spectrometry. However, most of them have some limitations. Surface plasmon resonance (SPR) spectroscopy was widely used in biosensing. However, its use to detect NTs is still growing and has fascinated impressive attention of the scientific community. The focus in this concise review paper will be on the principle of SPR sensors and its operation mechanism, the factors that affect the sensor performance. The efficiency of SPR biosensors to detect several clinically related analytes will be mentioned. DA functions in the human body will be explained. Additionally, this review will cover the incorporation of nanomaterials into SPR biosensors and its potential for DA sensing with mention to its advantages and disadvantages.
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2.
The "Sick-but-not-Dead" Phenomenon Applied to Catecholamine Deficiency in Neurodegenerative Diseases.
Goldstein, DS
Seminars in neurology. 2020;(5):502-514
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Abstract
The catecholamines dopamine and norepinephrine are key central neurotransmitters that participate in many neurobehavioral processes and disease states. Norepinephrine is also the main neurotransmitter mediating regulation of the circulation by the sympathetic nervous system. Several neurodegenerative disorders feature catecholamine deficiency. The most common is Parkinson's disease (PD), in which putamen dopamine content is drastically reduced. PD also entails severely decreased myocardial norepinephrine content, a feature that characterizes two other Lewy body diseases-pure autonomic failure and dementia with Lewy bodies. It is widely presumed that tissue catecholamine depletion in these conditions results directly from loss of catecholaminergic neurons; however, as highlighted in this review, there are also important functional abnormalities in extant residual catecholaminergic neurons. We refer to this as the "sick-but-not-dead" phenomenon. The malfunctions include diminished dopamine biosynthesis via tyrosine hydroxylase (TH) and L-aromatic-amino-acid decarboxylase (LAAAD), inefficient vesicular sequestration of cytoplasmic catecholamines, and attenuated neuronal reuptake via cell membrane catecholamine transporters. A unifying explanation for catecholaminergic neurodegeneration is autotoxicity exerted by 3,4-dihydroxyphenylacetaldehyde (DOPAL), an obligate intermediate in cytoplasmic dopamine metabolism. In PD, putamen DOPAL is built up with respect to dopamine, associated with a vesicular storage defect and decreased aldehyde dehydrogenase activity. Probably via spontaneous oxidation, DOPAL potently oligomerizes and forms quinone-protein adducts with ("quinonizes") α-synuclein (AS), a major constituent in Lewy bodies, and DOPAL-induced AS oligomers impede vesicular storage. DOPAL also quinonizes numerous intracellular proteins and inhibits enzymatic activities of TH and LAAAD. Treatments targeting DOPAL formation and oxidation therefore might rescue sick-but-not-dead catecholaminergic neurons in Lewy body diseases.
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Putative COVID- 19 Induction of Reward Deficiency Syndrome (RDS) and Associated Behavioral Addictions with Potential Concomitant Dopamine Depletion: Is COVID-19 Social Distancing a Double Edged Sword?
Blum, K, Cadet, JL, Baron, D, Badgaiyan, RD, Brewer, R, Modestino, EJ, Gold, MS
Substance use & misuse. 2020;(14):2438-2442
Abstract
The overwhelming fatalities of the global COVID-19 Pandemic will have daunting epigenetic sequala that can translate into an array of mental health issues, including panic, phobia, health anxiety, sleep disturbances to dissociative like symptoms including suicide. Method: We searched PUBMED for articles listed using the search terms "COVID 19 Pandemic", COVID19 and genes," "stress and COVID 19", Stress and Social distancing: Results: Long-term social distancing may be neurologically harmful, the consequence of epigenetic insults to the gene encoding the primary receptor for SARS-CoV2, and COVID 19. The gene is Angiotensin I Converting-Enzyme 2 (ACE2). According to the multi-experiment matrix (MEM), the gene exhibiting the most statistically significant co-expression link to ACE2 is Dopa Decarboxylase (DDC). DDC is a crucial enzyme that participates in the synthesis of both dopamine and serotonin. SARS-CoV2-induced downregulation of ACE2 expression might reduce dopamine and serotonin synthesis, causing hypodopaminergia. Discussion: Indeed, added to the known reduced dopamine function during periods of stress, including social distancing the consequence being both genetic and epigenetic vulnerability to all Reward Deficiency Syndrome (RDS) addictive behaviors. Stress seen in PTSD can generate downstream alterations in immune functions by reducing methylation levels of immune-related genes. Conclusion: Mitigation of these effects by identifying subjects at risk and promoting dopaminergic homeostasis to help regulate stress-relative hypodopaminergia, attenuate fears, and prevent subsequent unwanted drug and non-drug RDS type addictive behaviors seems prudent.
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4.
Neurochemical features of idiopathic restless legs syndrome.
Jiménez-Jiménez, FJ, Alonso-Navarro, H, García-Martín, E, Agúndez, JAG
Sleep medicine reviews. 2019;:70-87
Abstract
The most important traditional hypotheses of the pathogenesis of idiopathic restless legs syndrome (iRLS) involve dopaminergic dysfunction and iron deficiency. However, a possible role of other neurotransmitter or neuromodulators, mainly glutamate, gamma-hydroxybutyric acid (GABA), and adenosine have been suggested in recent reports. Moreover, iron deficiency in experimental models (which causes sensorimotor symptoms resembling those of RLS) is able to induce changes in dopaminergic, glutamatergic and adenosinergic neurotransmission, thus suggesting its crucial role in the pathogenesis of this disease. Relationship between iRLS and opiates, oxidative stress and nitric oxide, and with vitamin D deficiency has also been reported, although data regarding these variables should be considered as preliminary. In this review, we focus on studies relating to neurochemical findings in iRLS.
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5.
Mean Diffusivity in the Dopaminergic System and Neural Differences Related to Dopaminergic System.
Takeuchi, H, Kawashima, R
Current neuropharmacology. 2018;(4):460-474
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Abstract
BACKGROUND The mean diffusivity (MD) parameter obtained by diffusion tensor imaging provides a measure of how freely water molecules move in brain tissue. Greater tissue density conferred by closely arrayed cellular structures is assumed to lower MD by inhibiting the free diffusion of water molecules. METHODS In this paper, we review studies showing MD variation among regions of the brain dopaminergic system (MDDS), especially subcortical structures such as the putamen, caudate nucleus, and globus pallidus, in different conditions with known associations to dopaminergic system function or dysfunction. The methodologies and background related to MD and MDDS are also discussed. RESULTS Past studies indicate that MDDS is sensitive to pathological derangement of dopaminergic activity, neural changes caused by cognitive and pharmacological interventions that are known to affect the dopaminergic system, and individual character traits related to dopaminergic function. CONCLUSION These results suggest that MDDS can be one useful tool to tap the neural differences related to the dopaminergic system.
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THE RESTLESS LEGS SYNDROME (REVIEW).
Japaridze, G, Kasradze, S, Maisuradze, L, Popp, R, Wetter, T
Georgian medical news. 2018;(285):74-81
Abstract
The restless legs syndrome (RLS), also known as Willis-Ekbom disease, is a common sleep related neurological disorder with prevalence between 1 and 10%, increasing with age. Women are more frequently affected than men. RLS is characterized by an urge to move the legs accompanied by uncomfortable and unpleasant sensations in the legs, worsening of complaints during periods of rest, improvement by movement and an increase of symptoms in the evening or at night. In addition, affected patients may also suffer from severe sleep disorders and negative effects on daily activities. There is often a history of RLS among first-degree relatives, especially with the primary form. Among other, comorbidities or causal factors are iron deficiency, terminal renal insufficiency, pregnancy, polyneuropathy, or psychotropic drugs. The etiology of primary (idiopathic) RLS has not been clarified yet; however, genetic factors and dysfunctional dopaminergic neurotransmission as well as alterations of central iron metabolism play an important role. In addition to non-pharmacological treatment such as lifestyle modifications or behavioral strategies, levodopa, dopamine agonists, or anticonvulsants are effective. Opioids may be used in otherwise refractory forms. In the case of secondary or comorbid RLS, treatment of the underlying disease is necessary.
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Striatal dopamine in Parkinson disease: A meta-analysis of imaging studies.
Kaasinen, V, Vahlberg, T
Annals of neurology. 2017;(6):873-882
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Abstract
A meta-analysis of 142 positron emission tomography and single photon emission computed tomography studies that have investigated striatal presynaptic dopamine function in Parkinson disease (PD) was performed. Subregional estimates of striatal dopamine metabolism are presented. The aromatic L-amino-acid decarboxylase (AADC) defect appears to be consistently smaller than the dopamine transporter and vesicular monoamine transporter 2 defects, suggesting upregulation of AADC function in PD. The correlation between disease severity and dopamine loss appears linear, but the majority of longitudinal studies point to a negative exponential progression pattern of dopamine loss in PD. Ann Neurol 2017;82:873-882.
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Dopamine dysregulation syndrome in Parkinson's disease: a systematic review of published cases.
Warren, N, O'Gorman, C, Lehn, A, Siskind, D
Journal of neurology, neurosurgery, and psychiatry. 2017;(12):1060-1064
Abstract
OBJECTIVES Dopamine dysregulation syndrome (DDS) is an uncommon complication of the treatment of Parkinson's disease, characterised by addictive behaviour and excessive use of dopaminergic medication. DDS may frequently go unrecognised or misdiagnosed. We aimed to clarify current understanding of presentation, risk factors, comorbidities and management of DDS. METHODS Case reports were identified through a systematic search of databases (PubMed, Embase) with the following terms: dopaminergic dysregulation syndrome, hedonistic homeostatic dysregulation, dopamine/levodopa addiction. RESULTS We reviewed 390 articles, identifying 98 cases of DDS. Early-onset Parkinson's disease (67%) and male gender (83%) were common. DDS presented with significant physical and social impairment, actions to enable or prevent detection of overuse, as well as mood, anxiety and motor fluctuations. All DDS cases met DSM-V (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) substance use disorder criteria. Past substance and psychiatric history was present in 15.3% and 10.2% of cases. Comorbid impulse control disorders (61%), psychosis (32%) and panic attacks (14%) were common. A large variety of management strategies were used; only 56% of cases resolving. Sodium valproate was successful in 5/5 cases. The response to deep brain stimulation varied. CONCLUSIONS Given the functional impairment, medical and psychiatric consequences and the difficulties of treatment, early identification of DDS should be a priority.
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Human Laboratory Studies on Cannabinoids and Psychosis.
Sherif, M, Radhakrishnan, R, D'Souza, DC, Ranganathan, M
Biological psychiatry. 2016;(7):526-38
Abstract
Some of the most compelling evidence supporting an association between cannabinoid agonists and psychosis comes from controlled laboratory studies in humans. Randomized, double-blind, placebo-controlled, crossover laboratory studies demonstrate that cannabinoid agonists, including phytocannabinoids and synthetic cannabinoids, produce a wide range of positive, negative, and cognitive symptoms and psychophysiologic deficits in healthy human subjects that resemble the phenomenology of schizophrenia. These effects are time locked to drug administration, are dose related, and are transient and rarely necessitate intervention. The magnitude of effects is similar to the effects of ketamine but qualitatively distinct from other psychotomimetic drugs, including ketamine, amphetamine, and salvinorin A. Cannabinoid agonists have also been shown to transiently exacerbate symptoms in individuals with schizophrenia in laboratory studies. Patients with schizophrenia are more vulnerable than healthy control subjects to the acute behavioral and cognitive effects of cannabinoid agonists and experience transient exacerbation of symptoms despite treatment with antipsychotic medications. Furthermore, laboratory studies have failed to demonstrate any "beneficial" effects of cannabinoid agonists in individuals with schizophrenia-challenging the cannabis self-medication hypothesis. Emerging evidence suggests that polymorphisms of several genes related to dopamine metabolism (e.g., COMT, DAT1, and AKT1) may moderate the effects of cannabinoid agonists in laboratory studies. Cannabinoid agonists induce dopamine release, although the magnitude of release does not appear to be commensurate to the magnitude and spectrum of their acute psychotomimetic effects. Interactions between the endocannabinoid, gamma-aminobutyric acid, and glutamate systems and their individual and interactive effects on neural oscillations provide a plausible mechanism underlying the psychotomimetic effects of cannabinoids.
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[Nicotine and caffeine: influence on dopaminergic transmission].
Napierała, M, Bogusiewicz, J, Enko, J, Florek, E
Przeglad lekarski. 2016;(10):791-4
Abstract
Dopamine plays an important role in the neuronal regulation of motivation / reward, voluntary movements, cognitive processes and the process of addiction. Disorders of the production and release of dopamine can be the base of the pathomechanism of many diseases. Both nicotine and caffeine are psychomotor stimulants. Caffeine, through inhibition of adenosine, increases the activity of the dopaminergic system, and it shows the reinforcing and the psychomotor effect. Nicotine gets its reinforcing and psychostimulant effects from blocking dopamine uptake and increasing synaptic dopamine release. Nicotine and caffeine affect the release of the dopamine. It is believed that the interaction of these substances may be a synergistic effect on pain perception, voluntary movement functions or behavioral traits.