Dopamine in Parkinson's disease

Latif, Saad; Jahangeer, Muhammad; Razia, Dure Maknoon; Ashiq, Mehvish; Ghaffar, Abdul; Akram, Muhammad; Allam, Aicha El; Bouyahya, Abdelhakim; Garipova, Larisa; Shariati, Mohammad Ali; Thiruvengadam, Muthu; Ansari, Mohammad Azam

doi:10.1016/j.cca.2021.08.009

Cited by 111 publications

(71 citation statements)

References 97 publications

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“…Over the past decades, much research has been carried out on mDA neurons, generally focused on investigating their role in neurological and psychiatric disorders, such as Parkinson’s disease, schizophrenia, and attention deficit hyperactivity disorder [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…In fact, DA plays an important role, other than in the neuromodulation of motor control, emotions, cognitive functions, also in awakening from sleep [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ]. It is known in fact that sleep disturbances occur in both schizophrenia and Parkinson’s disease (19,20).…”

Section: Discussionmentioning

confidence: 99%

“…Significantly lower levels of serotonin, a brain chemical involved in many functions, including the sleep-wake cycle regulation, have been observed in SIDS victims compared to the serotonin values found in infants who had died of known causes [ 11 , 12 ]. However, to date, no research has yet been carried out on the possible implication in the pathophysiology of SIDS of dopamine (DA) which, on the contrary, is one of the most-studied neurotransmitters in many neurodegenerative disorders, due to its fundamental role in neuromodulation of various biological processes, such as motor control, cognitive function and sleep–wake cycle regulation [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ]. In particular, loss of midbrain dopaminergic (mDA) neurons, which are the main source of DA in the mammalian central nervous system, has been associated with alterations in arousal from sleep in patients with Parkinson’s disease [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Altered Development of Mesencephalic Dopaminergic Neurons in SIDS: New Insights into Understanding Sudden Infant Death Pathogenesis

Lavezzi

2021

Biomedicines

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Sudden infant death syndrome (SIDS) is defined as the unexpected sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation. The SIDS pathogenesis is still unknown; however, abnormalities in brain centers that control breathing and arousal from sleep, including dramatic changes in neurotransmitter levels, have been supposed in these deaths. This is the first study focusing on mesencephalic dopaminergic neurons, so far extensively studied only in animals and human neurological diseases, in SIDS. Dopaminergic structures in midbrain sections of a large series of sudden infant deaths (36 SIDS and 26 controls) were identified using polyclonal rabbit antibodies against tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, and the dopamine transporter, a membrane protein specifically expressed in dopaminergic cells. Dopamine-immunolabeled neurons were observed concentrated in two specific structures: the pars compacta of the substantia nigra and in the subnucleus medialis of the periaqueductal gray matter. Anatomical and functional degenerations of dopaminergic neurons in these regions were observed in most SIDS cases but never in controls. These results indicate that dopamine depletion, which is already known to be linked especially to Parkinson’s disease, is strongly involved even in SIDS pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Altered Development of Mesencephalic Dopaminergic Neurons in SIDS: New Insights into Understanding Sudden Infant Death Pathogenesis

Lavezzi

2021

Biomedicines

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“…In addition, loss of dopaminergic neurons in the ventral tegmental area (VTA) of the midbrain, which form mesolimbic and mesocortical projections, causes non-motor symptoms, such as emotional and cognitive impairment. Interestingly, however, the degenerative processes in the VTA are milder and slower, suggestive of different mechanisms operating [ 4 , 5 , 6 , 7 ]. Mitochondrial dysfunction [ 8 , 9 ] and alpha-synuclein deposition [ 10 , 11 ] are thought to play pivotal roles.…”

Section: Introductionmentioning

confidence: 99%

“…In Parkinson disease, the possibility of disease-modifying therapy using Ca 2+ channel blockers that inhibit neuronal excitability has been suggested [ 23 , 24 , 25 ]. Moreover, milder and slower neurodegenerative processes of dopaminergic neurons in the VTA may reflect less Ca 2+ -related oxidative stress as compared with those in the substantia nigra [ 4 , 5 , 6 , 7 ]. The distribution of amyloid-beta accumulation in the brain, which underlies the pathogenesis of Alzheimer disease, has also been linked to neural activity [ 26 , 27 ].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease

Takahashi

Mashima

2022

Antioxidants

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Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and solitary disease forms and is often unclear. In addition to the pathogenicity of alpha-synuclein as a pathological disease marker, the involvement of dopamine itself and its interactions with glial cells (astrocyte or microglia) have attracted attention. Pacemaking activity, which is a hallmark of dopaminergic neurons, is essential for the homeostatic maintenance of adequate dopamine concentrations in the synaptic cleft, but it imposes a burden on mitochondrial oxidative glucose metabolism, leading to reactive oxygen species production. Astrocytes provide endogenous neuroprotection to the brain by producing and releasing antioxidants in response to oxidative stress. Additionally, the protective function of astrocytes can be modified by microglia. Some types of microglia themselves are thought to exacerbate Parkinson disease by releasing pro-inflammatory factors (M1 microglia). Although these inflammatory microglia may further trigger the inflammatory conversion of astrocytes, microglia may induce astrocytic neuroprotective effects (A2 astrocytes) simultaneously. Interestingly, both astrocytes and microglia express dopamine receptors, which are upregulated in the presence of neuroinflammation. The anti-inflammatory effects of dopamine receptor stimulation are also attracting attention because the functions of astrocytes and microglia are greatly affected by both dopamine depletion and therapeutic dopamine replacement in Parkinson disease. In this review article, we will focus on the antioxidative and anti-inflammatory effects of astrocytes and their synergism with microglia and dopamine.

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Metabolomics study based on GC–MS reveals a protective function of luteolin against glutamate‐induced PC12 cell injury

Gao

Zhu

Sun

et al. 2022

Biomedical Chromatography

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Oxidative stress response is closely related to neurodegenerative diseases. This study aimed to investigate the cytoprotective effects of luteolin on glutamate‐induced oxidative stress injury in PC12 cells. GC–MS combined with multivariate statistical approaches was used to perform metabolomics studies to assess the possible mechanisms. Our results identified 23 metabolites as differential expressed metabolites in the glutamate group, including cysteine content in cells that decreased drastically. This suggests that glutathione synthesis, which balances the redox state of cells, was affected. Luteolin inhibits the reduction in viability in glutamate‐induced PC12 cells and regulates 13 differential expressed metabolites in glutamate‐induced cell damage. These metabolites associated with luteolin included glycine, serine, and threonine metabolism; glyoxylate and dicarboxylate metabolism; aminoacyl‐tRNA biosynthesis; cysteine and methionine metabolism; inositol phosphate metabolism; and starch and sucrose metabolism. In summary, the systemic antioxidant capacity of luteolin in PC12 cells is related to its regulation of amino acid, glucose, and nucleotide metabolism pathways.

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Dopamine in Parkinson's disease

Cited by 111 publications

References 97 publications

Altered Development of Mesencephalic Dopaminergic Neurons in SIDS: New Insights into Understanding Sudden Infant Death Pathogenesis

Altered Development of Mesencephalic Dopaminergic Neurons in SIDS: New Insights into Understanding Sudden Infant Death Pathogenesis

Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease

Metabolomics study based on GC–MS reveals a protective function of luteolin against glutamate‐induced PC12 cell injury

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