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  1. Book ; Online ; E-Book: NeuroPsychopharmacotherapy

    Riederer, Peter / Laux, Gerd / Nagatsu, Toshiharu / Le, Weidong / Riederer, Christian

    (Springer nature reference)

    2022  

    Abstract: Vol 1. Basic Principles and General Aspects -- Vol 2. Classes, Drugs and Special Aspects -- Vol 3. Applied Psychopharmacotherapy. ...

    Author's details edited by Peter Riederer, Gerd Laux, Toshiharu Nagatsu, Weidong Le, Christian Riederer
    Series title Springer nature reference
    Abstract Vol 1. Basic Principles and General Aspects -- Vol 2. Classes, Drugs and Special Aspects -- Vol 3. Applied Psychopharmacotherapy.
    Keywords Neurology ; Psychiatry ; Medical sciences ; Psychology ; Neurochemistry
    Language English
    Size 1 Online-Ressource (lviii, 4725 Seiten), Illustrationen, Diagramme
    Edition First edition
    Publisher Springer International Publishing ; Imprint: Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021735347
    ISBN 978-3-030-62059-2 ; 9783030620585 ; 3-030-62059-X ; 3030620581
    DOI 10.1007/978-3-030-62059-2
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view.

    Sian-Hulsmann, Jeswinder / Riederer, Peter

    Journal of neural transmission (Vienna, Austria : 1996)

    2024  

    Abstract: Fascinatingly, an abundance of recent studies has subscribed to the importance of cytotoxic immune mechanisms that appear to increase the risk/trigger for many progressive neurodegenerative disorders, including Parkinson's disease (PD), Alzheimer's ... ...

    Abstract Fascinatingly, an abundance of recent studies has subscribed to the importance of cytotoxic immune mechanisms that appear to increase the risk/trigger for many progressive neurodegenerative disorders, including Parkinson's disease (PD), Alzheimer's disease (AD), amyotrophic lateral sclerosis, and multiple sclerosis. Events associated with the neuroinflammatory cascades, such as ageing, immunologic dysfunction, and eventually disruption of the blood-brain barrier and the "cytokine storm", appear to be orchestrated mainly through the activation of microglial cells and communication with the neurons. The inflammatory processes prompt cellular protein dyshomeostasis. Parkinson's and Alzheimer's disease share a common feature marked by characteristic pathological hallmarks of abnormal neuronal protein accumulation. These Lewy bodies contain misfolded α-synuclein aggregates in PD or in the case of AD, they are Aβ deposits and tau-containing neurofibrillary tangles. Subsequently, these abnormal protein aggregates further elicit neurotoxic processes and events which contribute to the onset of neurodegeneration and to its progression including aggravation of neuroinflammation. However, there is a caveat for exclusively linking neuroinflammation with neurodegeneration, since it's highly unlikely that immune dysregulation is the only factor that contributes to the manifestation of many of these neurodegenerative disorders. It is unquestionably a complex interaction with other factors such as genetics, age, and environment. This endorses the "multiple hit hypothesis". Consequently, if the host has a genetic susceptibility coupled to an age-related weakened immune system, this makes them more susceptible to the virus/bacteria-related infection. This may trigger the onset of chronic cytotoxic neuroinflammatory processes leading to protein dyshomeostasis and accumulation, and finally, these events lead to neuronal destruction. Here, we differentiate "neuroinflammation" and "inflammation" with regard to the involvement of the blood-brain barrier, which seems to be intact in the case of neuroinflammation but defect in the case of inflammation. There is a neuroinflammation-inflammation continuum with regard to virus-induced brain affection. Therefore, we propose a staging of this process, which might be further developed by adding blood- and CSF parameters, their stage-dependent composition and stage-dependent severeness grade. If so, this might be suitable to optimise therapeutic strategies to fight brain neuroinflammation in its beginning and avoid inflammation at all.
    Language English
    Publishing date 2024-01-23
    Publishing country Austria
    Document type Journal Article
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-023-02723-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Umbrella-Review zur Serotonin-Theorie der Depression: Kritik aus neurobiochemischer Sicht

    Riederer, Peter

    Psychopharmakotherapie

    2022  Volume 29, Issue 5, Page(s) 190

    Language German
    Document type Article
    ZDB-ID 1196510-1
    ISSN 0944-6877
    Database Current Contents Medicine

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  4. Article ; Online: Gerald Stern (1930-2018).

    Riederer, Peter

    Journal of neural transmission (Vienna, Austria : 1996)

    2020  Volume 127, Issue 5, Page(s) 699

    Language English
    Publishing date 2020-02-22
    Publishing country Austria
    Document type Editorial
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-020-02176-0
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  5. Article ; Online: Prof. Dr. Moussa B.H. Youdim: an appreciation on the occasion of his 80th birthday.

    Riederer, Peter

    Journal of neural transmission (Vienna, Austria : 1996)

    2020  Volume 127, Issue 2, Page(s) 117–118

    MeSH term(s) Anniversaries and Special Events ; History, 20th Century ; History, 21st Century ; Humans ; Neurosciences/history
    Language English
    Publishing date 2020-02-03
    Publishing country Austria
    Document type Biography ; Editorial ; Historical Article ; Personal Narrative
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-020-02153-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book: Monoamine oxidases and their inhibitors

    Youdim, Moussa B. H. / Riederer, Peter

    (International review of neurobiology ; 100)

    2011  

    Author's details ed. by Moussa B. H. Youdim ; Peter Riederer
    Series title International review of neurobiology ; 100
    Collection
    Language English
    Size XV, 281 S. : Ill., graph. Darst.
    Edition 1. ed.
    Publisher Elsevier AP
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT017067948
    ISBN 978-0-12-386467-3 ; 0-12-386467-4
    Database Catalogue ZB MED Medicine, Health

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    Ui II Zs 180 -100- verfügbar in Königswinter Königswinter

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  7. Article ; Online: The vicious circle between homocysteine, methyl group-donating vitamins and chronic levodopa intake in Parkinson's disease.

    Müller, Thomas / Riederer, Peter

    Journal of neural transmission (Vienna, Austria : 1996)

    2023  

    Abstract: A biomarker for declined methylation capacity is elevation of homocysteine levels. They increase the risk for onset of vascular disease and contribute to progression of chronic neurodegeneration and aging. This narrative review discusses associations ... ...

    Abstract A biomarker for declined methylation capacity is elevation of homocysteine levels. They increase the risk for onset of vascular disease and contribute to progression of chronic neurodegeneration and aging. This narrative review discusses associations between homocysteine, consumption of methyl group-donating vitamins and impact on disease-generating mechanisms in levodopa-treated patients with Parkinson's disease. We conclude to recommend levodopa-treated patients to substitute themselves with methyl group-donating vitamins. This is harmless in terms of application of folic acid, methylcobalamin or hydroxocobalamin. Moreover, we suggest a crucial discussion on the value of the various popular hypotheses on Parkinson's disease-generating mechanisms. Findings from studies with acute levodopa exposure describe oxidative stress generation and impaired methylation capacity, which causes gene dysfunction. Their repeated occurrences contribute to onset of mitochondrial dysfunction, iron enrichment and pathologic protein accumulation in the long term. Current research underestimates these epigenetic, metabolic consequences of chronic levodopa application. Supplementary treatment strategies are recommended to avoid levodopa-related side effects.
    Language English
    Publishing date 2023-06-17
    Publishing country Austria
    Document type Journal Article ; Review
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-023-02666-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: L-DOPA-therapy in Parkinson's disease: some personal reflections on L-DOPA therapy from Vienna and Berlin.

    Riederer, Peter / Horowski, Reinhard

    Journal of neural transmission (Vienna, Austria : 1996)

    2023  Volume 130, Issue 11, Page(s) 1323–1335

    Abstract: Dopamine was initially considered as a mere intermediate in the noradrenaline synthesis but was then found to be a neurotransmitter. Its depletion resulted in characteristic symptoms in experimental studies and could be antagonized by DOPA (3,4- ... ...

    Abstract Dopamine was initially considered as a mere intermediate in the noradrenaline synthesis but was then found to be a neurotransmitter. Its depletion resulted in characteristic symptoms in experimental studies and could be antagonized by DOPA (3,4-dihydroxyphenylalanin), suggesting a similarity to the human disorder Parkinson´s disease (PD) and a therapeutic potential which was successfully exploited from the 1970s on. This was due to the pioneering work of Arvid Carlsson and clinicians around the world who first worked on the breakthrough of L-DOPA therapy and then on its amendment and modification and on alternative therapies for PD patients. All these developments led to the establishment of PD therapy as we know it today. It is characterized by the availability of many different compounds which are mostly employed in combination and by different methods: orally, intravenously, transdermally, subcutaneously, or duodenally. Here, we present without claim of completeness some personal reflections about causal drug developments for PD patients and reflect on some personal interactions with leading clinicians and basic researchers who cooperated with us. Such interactions are crucial for the creation, sometimes serendipitously, of fresh ideas and to further develop existing concepts to make therapeutical progress.
    MeSH term(s) Humans ; Levodopa/therapeutic use ; Parkinson Disease/drug therapy ; Antiparkinson Agents/therapeutic use ; Berlin ; Dopamine
    Chemical Substances Levodopa (46627O600J) ; Antiparkinson Agents ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2023-10-05
    Publishing country Austria
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-023-02692-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.

    Sian-Hulsmann, Jeswinder / Riederer, Peter

    Journal of neural transmission (Vienna, Austria : 1996)

    2023  

    Abstract: Multiple System Atrophy (MSA) and Parkinson's diseases (PD) are elite members of the α-synucleinopathy organization. Aberrant accumulations of the protein α-synuclein characterize them. A plethora of evidence indicates the involvement of these rogue ... ...

    Abstract Multiple System Atrophy (MSA) and Parkinson's diseases (PD) are elite members of the α-synucleinopathy organization. Aberrant accumulations of the protein α-synuclein characterize them. A plethora of evidence indicates the involvement of these rogue inclusions in a cascade of events that disturb cellular homeostasis resulting in neuronal dysfunction. These two neurodegenerative diseases share many features both clinically and pathologically. Cytotoxic processes commonly induced by reactive free radical species have been associated with oxidative stress and neuroinflammation, frequently reported in both diseases. However, it appears they have characteristic and distinct α-synuclein inclusions. It is glial cytoplasmic inclusions in the case of MSA while Lewy bodies manifest in PD. This is probably related to the etiology of the illness. At present, precise mechanism(s) underlying the characteristic configuration of neurodegeneration are unclear. Furthermore, the "prion-like" transmission from cell to cell prompts the suggestion that perhaps these α-synucleinopathies are prion-like diseases. The possibility of some underlying genetic foul play remains controversial. But as major culprits of pathological processes or even single triggers of PD and MSA are the same-like oxidative stress, iron-induced pathology, mitochondriopathy, loss of respiratory activity, loss of proteasomal function, microglial activation, neuroinflammation-it is not farfetched to assume that in sporadic PD and also in MSA a variety of combinations of susceptibility genes contribute to the regional specificity of pathological onset. These players of pathology, as mentioned above, in a synergistic combination, are responsible for driving the progression of PD, MSA and other neurodegenerative disorders. Elucidating the triggers and progression factors is vital for advocating disease modification or halting its progression in both, MSA and PD.
    Language English
    Publishing date 2023-05-25
    Publishing country Austria
    Document type Journal Article ; Review
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-023-02653-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book: Grundlagen der Neuro-Psychopharmakologie

    Riederer, Peter / Laux, Gerd

    ein Therapiehandbuch

    2010  

    Author's details Peter F. Riederer, Gerd Laux (Hrsg.)
    Keywords Psychopharmakotherapie ; Neuropharmakologie ; Psychopharmakon
    Subject Psychopharmaka ; Psychotrope Substanz ; Psychotropische Substanz ; Psychotherapeutikum ; Nervensystem ; Psychopharmakon
    Language German
    Size VIII, 619 Seiten, Illustrationen
    Publisher Springer
    Publishing place Wien u.a.
    Publishing country Austria
    Document type Book
    HBZ-ID HT015699626
    ISBN 978-3-211-85472-3 ; 3-211-85472-X ; 9783211854730 ; 3211854738
    Database Catalogue ZB MED Medicine, Health

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    2009 A 5932 order for loan Magazin

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