Degenerative Diseases of the Nervous System
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Parkinsonism: Dopaminergic drugs: In order of effectiveness and lower risk–benefit ratio: levodopa, dopamine agonists (bromocriptine > pergolide > lisuride in older literature) may reduce the symptoms in some cases but a sustained response is rare.Amantadine may cause temporary improvement in a small subset of patients.Higher doses of levodopa may be needed for clinical response (up to 1 g daily).Levodopa-induced dyskinesias are rare, but dystonia may occur (dysarthria, apraxia of eyelid closure).Case reports of improvement in some patients with zolpidem, anticholinergics, idazoxan, tricyclic antidepressants, L-threo-3,4-dihydroxy-phenylserine (L-DOPS), methysergide.
Serotonin Metabolism in Functional Somatic Illness
Peter Manu in The Psychopathology of Functional Somatic Syndromes, 2020
The first investigation of serotonin metabolism in chronic fatigue syndrome was carried out at the National Institutes of Health, Bethesda, Maryland (Demitrack et al., 1992). The work assessed the central monoaminergic activity involved in serotonergic, noradrenergic, and dopaminergic neurotransmission. Nineteen patients (13 women and six men) with this syndrome and 17 healthy control subjects (eight women and nine men) underwent lumbar puncture and had their blood and cerebrospinal fluid tested for 5-hydroxyindoleacetic acid (the main metabolite of serotonin), 3-methoxy-4-hydroxyphenylglycol (the main metabolite of norepinephrine), and homovanillic acid (the main metabolite of dopamine). All patients were also administered a structured psychiatric interview.
Psychological determinants of substance misuse by young people
Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros in Substance Misuse and Young People, 2019
A second set of broadly psychological issues relates to addiction, which is a combination of an overriding compulsion to use a substance and symptoms of withdrawal when the substance is not available. The biological mechanism involves the subcortical dopaminergic reward centres discussed elsewhere in this book. In effect, addiction transfers control from the cortex to subcortical structures, which may account for the dehumanising effect of what Nora Volkow refers to as a ‘disease … of the striatothalamo-orbitofrontal circuit’ (Volkow and Fowler, 2000). Pronounced physiological withdrawal syndromes are unusual in young people who have not had sufficient time for dependency to emerge. However, compulsive drug-taking without marked withdrawals does seem to occur, particularly with stimulants that include novel psychoactive substances that generate ‘a downward cycle of bingeing and periods of recovery associated with depression’ (Advisory Council on the Misuse of Drugs, 2010).
Developmental exposure to the A6-pesticide causes changes in tyrosine hydroxylase gene expression, neurochemistry, and locomotors behavior in larval zebrafish
Published in Toxicology Mechanisms and Methods, 2022
Ahmed Nasri, Pierre-André Lafon, Amine Mezni, Philippe Clair, Nicolas Cubedo, Ezzeddine Mahmoudi, Hamouda Beyrem, Mireille Rossel, Véronique Perrier
To confirm the locomotors disturbance observed after treatment with the biopesticide A6 compared to the control (DMSO). Changes in the patterning of their dopaminergic neurons were examined at 6 dpf. The nomenclature used for the dopaminergic neurons was as described previously (Tay et al. 2011). Low doses of A6 resulted in appreciable changes in brain TH expression compared with that in the control (Figure 5). The first changes in neuronal patterning were observed in the olfactory bulb (OB) at all concentrations tested, where labeling of these neurons showed a decrease in fluorescence intensity (Figure 5(B–D)) in contrast to control (Figure 5(A)). The subpallium within the telencephalon (SP) also appears not to be altered by A6. In the pre-tectal (Pr) area, the density of neuronal labeling was not affected (Figure 5(F–H)) compared with that in the control DMSO group (Figure 5(E)). In addition, neuronal labeling in the area postrema (AP) showed a reduction with only the 50 nM of A6 (Figure 5(L)) compared with the control (Figure 5(I)).
Association of dopamine β-hydroxylase polymorphism rs1611115 and serum levels with psychiatric disorders in Pakistani population
Published in International Journal of Neuroscience, 2022
Aisha Nasir Hashmi, Raees Ahmed Dharejo, Usama Bin Zubair, Netasha Khan, Iqra Kashif, Muhammad Ajmal, Rizwan Taj, Raheel Qamar, Maleeha Azam
Dopamine β-hydroxylase (DBH) is a copper-containing enzyme of the dopaminergic system, which catalyzes the dopamine (DA) conversion into nor-adrenaline (NA) [1,2]. The dopaminergic system regulates mood, attention, motivation, reward system, decision making and psychomotor activity of the brain and DA is one of the important stimulatory neurotransmitters in this pathway [3]. The gene encoding DBH resides on chromosome 9q34, it has 12 exons and is approximately 23 kb in size [4,5]. The DBH is expressed in the locus-coeruleus part of the brain [6], and is localized in synaptic vesicles, of peripheral (noradrenergic) and central (noradrenergic and adrenergic) neurons and is also found in the neuro-secretory cells of the adrenal medulla [2,7]. Upon adrenergic stimulation, the DBH and NA are released from vesicles through exocytosis from the sympathetic neurons and the adrenal medulla and then enters into the blood circulation, where DBH can be detected in plasma/serum [8].
Effect of nutrition on neurodegenerative diseases. A systematic review
Published in Nutritional Neuroscience, 2021
Vittorio Emanuele Bianchi, Pomares Fredy Herrera, Rizzi Laura
Parkinson’s disease (PD) is characterized by neuronal degeneration due to a dopaminergic loss in the substantia nigra. The preliminary dysfunction in PD appears as motor neuron alteration, tremors, loss of muscular strength, and subsequent cognitive decline and dementia [13]. The dysfunction in PD may result from a reduction in dopaminergic, cholinergic, and other non-dopaminergic neurotransmitters, and structural deficiency, including hippocampal and cortical atrophy, especially of the posterior occipital cortices [14]. Dementia in PD is particularly prevalent in advanced age, resulting in high morbidity and mortality in approximately 80–90% of cases. The pathogenetic mechanisms of PD are not clearly explained, but recently, the insulin resistance has been evidenced [15,16] suggesting a correlation between the alteration of glucose metabolism with neurodegeneration.
Related Knowledge Centers
- Biosynthesis
- Dopamine Receptor
- Dopamine Transporter
- Dopaminergic Pathways
- Protein
- Synapse
- Dopamine
- Neurotransmitter
- Vesicular Monoamine Transporter 2
- Neuron