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Article: Multifunctional Metallothioneins as a Target for Neuroprotection in Parkinson's Disease.

Miyazaki, Ikuko / Asanuma, Masato

2023 Volume 12, Issue 4

Abstract: Parkinson's disease (PD) is characterized by motor symptoms based on a loss of nigrostriatal dopaminergic neurons and by non-motor symptoms which precede motor symptoms. Neurodegeneration accompanied by an accumulation of α-synuclein is thought to ... ...

Abstract	Parkinson's disease (PD) is characterized by motor symptoms based on a loss of nigrostriatal dopaminergic neurons and by non-motor symptoms which precede motor symptoms. Neurodegeneration accompanied by an accumulation of α-synuclein is thought to propagate from the enteric nervous system to the central nervous system. The pathogenesis in sporadic PD remains unknown. However, many reports indicate various etiological factors, such as oxidative stress, inflammation, α-synuclein toxicity and mitochondrial impairment, drive neurodegeneration. Exposure to heavy metals contributes to these etiopathogenesis and increases the risk of developing PD. Metallothioneins (MTs) are cysteine-rich metal-binding proteins; MTs chelate metals and inhibit metal-induced oxidative stress, inflammation and mitochondrial dysfunction. In addition, MTs possess antioxidative properties by scavenging free radicals and exert anti-inflammatory effects by suppression of microglial activation. Furthermore, MTs recently received attention as a potential target for attenuating metal-induced α-synuclein aggregation. In this article, we summarize MTs expression in the central and enteric nervous system, and review protective functions of MTs against etiopathogenesis in PD. We also discuss neuroprotective strategies for the prevention of central dopaminergic and enteric neurodegeneration by targeting MTs. This review highlights multifunctional MTs as a target for the development of disease-modifying drugs for PD.
Language	English
Publishing date	2023-04-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12040894
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Factors associated with cancer disclosure in adolescent and young adult cancer survivors: An integrative review from the social-ecological model perspective.

Honda, Naoko / Shiroshita, Yui / Miyazaki, Asuka / Sobue, Ikuko

European journal of oncology nursing : the official journal of European Oncology Nursing Society

2024 Volume 69, Page(s) 102542

Abstract: Purpose: Young cancer survivors ("young survivors") may need to disclose their cancer experiences to reintegrate into society. In such cases, the recognition of social support through the disclosure of cancer experiences may prevent potential social ... ...

Abstract	Purpose: Young cancer survivors ("young survivors") may need to disclose their cancer experiences to reintegrate into society. In such cases, the recognition of social support through the disclosure of cancer experiences may prevent potential social disadvantages． This review aimed to describe the motivations, strategies and outcomes, and benefits and disadvantages of disclosure in young survivors based on the social-ecological model (SEM) to identify the support survivors need when disclosing their cancer experiences. Methods: Using the integrated review methodology, we systematically searched six databases in English and Japanese as well as searched the reference lists of the selected studies. The themes identified via thematic analysis were categorized within the SEM levels. Results: This review analyzed 14 studies and identified four themes, including "Motivation for Cancer Disclosure," "Barriers to Cancer Disclosure," "Consequences of Cancer Disclosure: Benefits," and "Consequences of Cancer Disclosure: Disadvantages." Motivations for young survivors to disclose their cancer involved post-cancer differences, perceptions, relationships, and social context. In navigating barriers, including self-stigma, peer exclusion, and discrimination, they employed strategies such as reassurance and information limitation. Tailored disclosure strategies at each SEM level offered social and psychological benefits, however, disadvantages, including stress, vulnerability, employment issues, and limited insurance coverage, were experienced by young survivors due to cancer disclosure. Conclusions: To optimize the benefits of cancer disclosure for young survivors, addressing psychological burdens, enhancing disclosure skills, offering familial psychological support, and fostering public awareness of cancer are essential.
MeSH term(s)	Humans ; Young Adult ; Adolescent ; Disclosure ; Cancer Survivors/psychology ; Survivors ; Social Stigma ; Social Support ; Neoplasms/psychology
Language	English
Publishing date	2024-02-23
Publishing country	Scotland
Document type	Systematic Review ; Journal Article ; Review
ZDB-ID	2017117-1
ISSN	1532-2122 ; 1462-3889
ISSN (online)	1532-2122
ISSN	1462-3889
DOI	10.1016/j.ejon.2024.102542
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Article ; Online: Multifunctional Metallothioneins as a Target for Neuroprotection in Parkinson’s Disease

Miyazaki, Ikuko / Asanuma, Masato

Antioxidants. 2023 Apr. 06, v. 12, no. 4

2023

Abstract: Parkinson’s disease (PD) is characterized by motor symptoms based on a loss of nigrostriatal dopaminergic neurons and by non-motor symptoms which precede motor symptoms. Neurodegeneration accompanied by an accumulation of α-synuclein is thought to ... ...

Abstract	Parkinson’s disease (PD) is characterized by motor symptoms based on a loss of nigrostriatal dopaminergic neurons and by non-motor symptoms which precede motor symptoms. Neurodegeneration accompanied by an accumulation of α-synuclein is thought to propagate from the enteric nervous system to the central nervous system. The pathogenesis in sporadic PD remains unknown. However, many reports indicate various etiological factors, such as oxidative stress, inflammation, α-synuclein toxicity and mitochondrial impairment, drive neurodegeneration. Exposure to heavy metals contributes to these etiopathogenesis and increases the risk of developing PD. Metallothioneins (MTs) are cysteine-rich metal-binding proteins; MTs chelate metals and inhibit metal-induced oxidative stress, inflammation and mitochondrial dysfunction. In addition, MTs possess antioxidative properties by scavenging free radicals and exert anti-inflammatory effects by suppression of microglial activation. Furthermore, MTs recently received attention as a potential target for attenuating metal-induced α-synuclein aggregation. In this article, we summarize MTs expression in the central and enteric nervous system, and review protective functions of MTs against etiopathogenesis in PD. We also discuss neuroprotective strategies for the prevention of central dopaminergic and enteric neurodegeneration by targeting MTs. This review highlights multifunctional MTs as a target for the development of disease-modifying drugs for PD.
Keywords	central nervous system ; etiology ; inflammation ; mitochondria ; neurodegenerative diseases ; neuroprotective effect ; oxidative stress ; pathogenesis ; risk ; toxicity
Language	English
Dates of publication	2023-0406
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12040894
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Editorial: Astrocyte-Targeted Therapeutic Strategies for Neurological Disorders.

Miyazaki, Ikuko

Current pharmaceutical design

2017 Volume 23, Issue 33, Page(s) 4933–4935

MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/pathology ; Humans ; Nervous System Diseases/drug therapy ; Nervous System Diseases/metabolism ; Nervous System Diseases/pathology ; Neuroprotection/drug effects ; Neuroprotection/physiology ; Neuroprotective Agents/administration & dosage
Chemical Substances	Neuroprotective Agents
Language	English
Publishing date	2017-10-11
Publishing country	United Arab Emirates
Document type	Editorial
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161282333180110125544
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 4714: Show issues

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Article ; Online: Glutathione and Related Molecules in Parkinsonism.

Asanuma, Masato / Miyazaki, Ikuko

International journal of molecular sciences

2021 Volume 22, Issue 16

Abstract: Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate cysteine readily becomes the oxidized dimeric cystine. Since neurons lack a cystine transport system, neuronal GSH synthesis depends on cystine ... ...

Abstract	Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate cysteine readily becomes the oxidized dimeric cystine. Since neurons lack a cystine transport system, neuronal GSH synthesis depends on cystine uptake via the cystine/glutamate exchange transporter (xCT), GSH synthesis, and release in/from surrounding astrocytes. Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a detoxifying master transcription factor, is expressed mainly in astrocytes and activates the gene expression of various phase II drug-metabolizing enzymes or antioxidants including GSH-related molecules and metallothionein by binding to the antioxidant response element (ARE) of these genes. Accumulating evidence has shown the involvement of dysfunction of antioxidative molecules including GSH and its related molecules in the pathogenesis of Parkinson's disease (PD) or parkinsonian models. Furthermore, we found several agents targeting GSH synthesis in the astrocytes that protect nigrostriatal dopaminergic neuronal loss in PD models. In this article, the neuroprotective effects of supplementation and enhancement of GSH and its related molecules in PD pathology are reviewed, along with introducing new experimental findings, especially targeting of the xCT-GSH synthetic system and Nrf2-ARE pathway in astrocytes.
MeSH term(s)	Amino Acid Transport System y+/metabolism ; Animals ; Astrocytes/metabolism ; Carboxylic Ester Hydrolases/metabolism ; Disease Models, Animal ; Gene Expression Regulation ; Glutathione/metabolism ; Humans ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Parkinsonian Disorders/metabolism ; Signal Transduction
Chemical Substances	Amino Acid Transport System y+ ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; SLC7A11 protein, human ; Carboxylic Ester Hydrolases (EC 3.1.1.-) ; arylesterase (EC 3.1.1.2) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2021-08-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22168689
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: [Therapeutic strategy for Parkinson's disease: targeting zinc-binding protein in astrocytes].

Miyazaki, Ikuko / Asanuma, Masato

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2021 Volume 156, Issue 2, Page(s) 76–80

Abstract: Parkinson's disease (PD) is a progressive neurodegenerative disease with motor symptoms, such as tremor, akinesia/bradykinesia, rigidity and postural instability due to a loss of nigrostriatal dopaminergic neurons; PD patients also exhibit non-motor ... ...

Abstract	Parkinson's disease (PD) is a progressive neurodegenerative disease with motor symptoms, such as tremor, akinesia/bradykinesia, rigidity and postural instability due to a loss of nigrostriatal dopaminergic neurons; PD patients also exhibit non-motor symptoms, such as hyposmia, orthostatic hypotension and constipation, which precede motor symptoms. Pathologically, Lewy bodies and neurites, which contains α-synuclein, are observed in the central and peripheral nervous system. To date, it is hypothesized that PD pathology appears first in the olfactory bulb and the enteric nervous system, and propagates progressively through the substantia nigra to finally reach the cerebral cortex. Major medications at present are nosotropic treatments to improve motor dysfunction in PD. Therefore, development of disease-modifying drug is required to slow or prevent PD progression. Astrocytes are known to play an important role in the maintenance of the neuronal environment and exert neuroprotective effects by production of antioxidants and neurotrophic factors and clearing toxic molecules. In the previous study, we demonstrated that astrocytes produced antioxidative molecules metallothionein (MT)-1/2 in response to oxidative stress and protected dopaminergic neurons against oxidative stress. MTs are cysteine-rich proteins possessing antioxidative properties. MTs bind to metals such as zinc (Zn) and copper (Cu) and function in metal homeostasis and detoxification; MTs regulate Zn-mediated transcriptional activation of various genes. Recently, it is reported that MTs prevent Cu-induced aggregation of α-synuclein. In this article, we review a new therapeutic strategy of neuroprotection in PD by targeting MTs in astrocytes.
MeSH term(s)	Astrocytes ; Carrier Proteins ; Humans ; Neurodegenerative Diseases ; Parkinson Disease/drug therapy ; alpha-Synuclein
Chemical Substances	Carrier Proteins ; alpha-Synuclein ; zinc-binding protein
Language	Japanese
Publishing date	2021-01-11
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.20082
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 439: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Glutathione and Related Molecules in Parkinsonism

Masato Asanuma / Ikuko Miyazaki

International Journal of Molecular Sciences, Vol 22, Iss 8689, p

2021 Volume 8689

Abstract	Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate cysteine readily becomes the oxidized dimeric cystine. Since neurons lack a cystine transport system, neuronal GSH synthesis depends on cystine uptake via the cystine/glutamate exchange transporter (xCT), GSH synthesis, and release in/from surrounding astrocytes. Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a detoxifying master transcription factor, is expressed mainly in astrocytes and activates the gene expression of various phase II drug-metabolizing enzymes or antioxidants including GSH-related molecules and metallothionein by binding to the antioxidant response element (ARE) of these genes. Accumulating evidence has shown the involvement of dysfunction of antioxidative molecules including GSH and its related molecules in the pathogenesis of Parkinson’s disease (PD) or parkinsonian models. Furthermore, we found several agents targeting GSH synthesis in the astrocytes that protect nigrostriatal dopaminergic neuronal loss in PD models. In this article, the neuroprotective effects of supplementation and enhancement of GSH and its related molecules in PD pathology are reviewed, along with introducing new experimental findings, especially targeting of the xCT-GSH synthetic system and Nrf2–ARE pathway in astrocytes.
Keywords	glutathione ; neuroprotection ; parkinsonism ; astrocyte ; region specificity ; striatum ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Neuron-Astrocyte Interactions in Parkinson’s Disease

Ikuko Miyazaki / Masato Asanuma

Cells, Vol 9, Iss 2623, p

2020 Volume 2623

Abstract: Parkinson’s disease (PD) is the second most common neurodegenerative disease. PD patients exhibit motor symptoms such as akinesia/bradykinesia, tremor, rigidity, and postural instability due to a loss of nigrostriatal dopaminergic neurons. Although the ... ...

Abstract	Parkinson’s disease (PD) is the second most common neurodegenerative disease. PD patients exhibit motor symptoms such as akinesia/bradykinesia, tremor, rigidity, and postural instability due to a loss of nigrostriatal dopaminergic neurons. Although the pathogenesis in sporadic PD remains unknown, there is a consensus on the involvement of non-neuronal cells in the progression of PD pathology. Astrocytes are the most numerous glial cells in the central nervous system. Normally, astrocytes protect neurons by releasing neurotrophic factors, producing antioxidants, and disposing of neuronal waste products. However, in pathological situations, astrocytes are known to produce inflammatory cytokines. In addition, various studies have reported that astrocyte dysfunction also leads to neurodegeneration in PD. In this article, we summarize the interaction of astrocytes and dopaminergic neurons, review the pathogenic role of astrocytes in PD, and discuss therapeutic strategies for the prevention of dopaminergic neurodegeneration. This review highlights neuron-astrocyte interaction as a target for the development of disease-modifying drugs for PD in the future.
Keywords	astrocyte ; Parkinson’s disease ; dopaminergic neuron ; neuroinflammation ; neuroprotection ; α-synuclein ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Neuron-Astrocyte Interactions in Parkinson's Disease.

Miyazaki, Ikuko / Asanuma, Masato

Cells

2020 Volume 9, Issue 12

Abstract: Parkinson's disease (PD) is the second most common neurodegenerative disease. PD patients exhibit motor symptoms such as akinesia/bradykinesia, tremor, rigidity, and postural instability due to a loss of nigrostriatal dopaminergic neurons. Although the ... ...

Abstract	Parkinson's disease (PD) is the second most common neurodegenerative disease. PD patients exhibit motor symptoms such as akinesia/bradykinesia, tremor, rigidity, and postural instability due to a loss of nigrostriatal dopaminergic neurons. Although the pathogenesis in sporadic PD remains unknown, there is a consensus on the involvement of non-neuronal cells in the progression of PD pathology. Astrocytes are the most numerous glial cells in the central nervous system. Normally, astrocytes protect neurons by releasing neurotrophic factors, producing antioxidants, and disposing of neuronal waste products. However, in pathological situations, astrocytes are known to produce inflammatory cytokines. In addition, various studies have reported that astrocyte dysfunction also leads to neurodegeneration in PD. In this article, we summarize the interaction of astrocytes and dopaminergic neurons, review the pathogenic role of astrocytes in PD, and discuss therapeutic strategies for the prevention of dopaminergic neurodegeneration. This review highlights neuron-astrocyte interaction as a target for the development of disease-modifying drugs for PD in the future.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Astrocytes/metabolism ; Disease Progression ; Dopamine/metabolism ; Dopaminergic Neurons/metabolism ; Humans ; Inflammation ; Mitochondria/metabolism ; Nerve Degeneration/pathology ; Neuroglia/metabolism ; Neurons/metabolism ; Neuroprotection ; Oxidative Stress ; Parkinson Disease/metabolism ; Signal Transduction ; alpha-Synuclein/metabolism
Chemical Substances	Antioxidants ; alpha-Synuclein ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2020-12-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9122623
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: [Anti-oxidants in astrocytes as target of neuroprotection for Parkinson's disease].

Asanuma, Masato / Miyazaki, Ikuko

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2020 Volume 156, Issue 1, Page(s) 14–20

Abstract: Recently, it has been reported that dysfunction of astrocytes is involved vulnerability of neuronal cells in several neurological disorders. Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate ... ...

Abstract	Recently, it has been reported that dysfunction of astrocytes is involved vulnerability of neuronal cells in several neurological disorders. Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate cysteine is readily becomes the oxidized dimeric cystine. Since neurons lack a cystine transport system, neuronal GSH synthesis depends on cystine uptake via the cystine/glutamate exchange transporter (xCT), GSH synthesis and release in/from surrounding astrocytes. The expression and release of the zinc-binding protein metallothionein (MT) in astrocytes, which is a strong antioxidant, is induced and exerts neuroprotective in the case of dopaminergic neuronal damage. In addition, the transcription factor Nrf2 induces expression of MT-1 and GSH related molecules. We previously revealed that several antiepileptic drugs, serotonin 5-HT1A receptor agonists, plant-derived chemicals (phytochemicals) increased xCT expression, Nrf2 activation, GSH or MT expression and release in/from astrocytes, and exerted a neuroprotective effect against dopaminergic neurodegeneration in Parkinson's disease model. Our serial studies on neuroprotection via antioxidant defense mechanism of astrocytes have found three target molecular systems of astrocytes for neuroprotection: (1) xCT-GSH synthetic system, (2) Nrf2 system and (3) 5-HT1A receptor-Nrf2-MT system, 5-HT1A-S100β system. In this article, possible neuroprotective strategy for Parkinson's disease has been reviewed targeting antioxidative molecules in astrocytes.
MeSH term(s)	Antioxidants/pharmacology ; Astrocytes ; Glutathione ; Humans ; Neuroprotection ; Neuroprotective Agents/pharmacology ; Parkinson Disease/drug therapy
Chemical Substances	Antioxidants ; Neuroprotective Agents ; Glutathione (GAN16C9B8O)
Language	Japanese
Publishing date	2020-12-01
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.20071
Database	MEDical Literature Analysis and Retrieval System OnLINE

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