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Impaired iron homeostasis in Parkinson's disease.

Overview of attention for book
Cover of 'Impaired iron homeostasis in Parkinson's disease.'

Table of Contents

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    Book Overview
  2. Altmetric Badge
    Chapter 1 The L -DOPA story revisited. Further surprises to be expected?
  3. Altmetric Badge
    Chapter 2 The enigma of cell death in neurodegenerative disorders
  4. Altmetric Badge
    Chapter 3 Impaired iron homeostasis in Parkinson’s disease
  5. Altmetric Badge
    Chapter 4 The molecular mechanism of dopamine-induced apoptosis: identification and characterization of genes that mediate dopamine toxicity
  6. Altmetric Badge
    Chapter 5 Glyceraldehyde-3-phosphate dehydrogenase in neurodegeneration and apoptosis signaling
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    Chapter 6 Importance of familial Parkinson’s disease and parkinsonism to the understanding of nigral degeneration in sporadic Parkinson’s disease
  8. Altmetric Badge
    Chapter 7 cDNA microarray to study gene expression of dopaminergic neurodegeneration and neuroprotection in MPTP and 6-hydroxydopamine models: implications for idiopathic Parkinson’s disease
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    Chapter 8 Monitoring neuroprotection and restorative therapies in Parkinson’s disease with PET
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    Chapter 9 Common properties for propargylamines of enhancing superoxide dismutase and catalase activities in the dopaminergic system in the rat: implications for the life prolonging effect of (–)deprenyl
  11. Altmetric Badge
    Chapter 10 TV3326, a novel neuroprotective drug with cholinesterase and monoamine oxidase inhibitory activities for the treatment of Alzheimer's disease.
  12. Altmetric Badge
    Chapter 11 Neurotoxins induce apoptosis in dopamine neurons: protection by N-propargylamine-1(R)- and (S)-aminoindan, rasagiline and TV1022
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    Chapter 12 Homocysteine and alcoholism
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    Chapter 13 Neurorescuing effects of the GAPDH ligand CGP 3466B.
  15. Altmetric Badge
    Chapter 14 The neuroprotective effects of CGP 3466B in the best in vivo model of Parkinson's disease, the bilaterally MPTP-treated rhesus monkey.
  16. Altmetric Badge
    Chapter 15 Neurotrophic effects of central nicotinic receptor activation
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    Chapter 16 Regulation of neuronal cell death and differentiation by NGF and IAP family members
  18. Altmetric Badge
    Chapter 17 Insulin-like growth factor-1 (IGF-1): a neuroprotective trophic factor acting via the Akt kinase pathway
  19. Altmetric Badge
    Chapter 18 GDF-15/MIC-1 a novel member of the TGF-ß superfamily
  20. Altmetric Badge
    Chapter 19 Changes in cytokines and neurotrophins in Parkinson’s disease
  21. Altmetric Badge
    Chapter 20 Psychiatric complications in Parkinson’s disease
  22. Altmetric Badge
    Chapter 21 Dementia with Lewy bodies: prevalence, clinical spectrum and natural history
  23. Altmetric Badge
    Chapter 22 Neuronal degeneration and reorganization: a mutual principle in pathological and in healthy interactions of limbic and prefrontal circuits
  24. Altmetric Badge
    Chapter 23 Depression in alpha-synucleinopathies: prevalence, pathophysiology and treatment
  25. Altmetric Badge
    Chapter 24 The serotonin transporter in Alzheimer’s and Parkinson’s disease
  26. Altmetric Badge
    Chapter 25 Immunopathogenic and clinical relevance of antibodies against myelin oligodendrocyte glycoprotein (MOG) in Multiple Sclerosis
  27. Altmetric Badge
    Chapter 26 Lessons from studies of antigen-specific T cell responses in Multiple Sclerosis
  28. Altmetric Badge
    Chapter 27 Glutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?
  29. Altmetric Badge
    Chapter 28 Evidence for enhanced neuro-inflammatory processes in neurodegenerative diseases and the action of nitrones as potential therapeutics
Overall attention for this book and its chapters
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (83rd percentile)
  • High Attention Score compared to outputs of the same age and source (80th percentile)

Mentioned by

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4 Wikipedia pages

Citations

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Title
Impaired iron homeostasis in Parkinson's disease.
Published by
Journal of neural transmission Supplementum, January 2000
DOI 10.1007/978-3-7091-6301-6
Pubmed ID
ISBNs
978-3-21-183538-8, 978-3-21-183537-1, 978-3-70-916301-6
Authors

Double, K L, Gerlach, M, Youdim, M B, Riederer, P

Editors

Riederer, P., Calne, D.B., Horowski, R., Mizuno, Y., Olanow, C.W., Poewe, W., Youdim, M.B.H.

Abstract

Despite physiological systems designed to achieve iron homeostasis, increased concentrations of brain iron have been demonstrated in a range of neurodegenerative diseases. These including the parkinsonian syndromes, the trinucleotide repeat disorders and the dementia syndromes. The increased brain iron is confined to those brain regions most affected by the degeneration characteristic of the particular disorder and is suggested to stimulate cell damage via oxidative mechanisms. Changes in central iron homeostasis have been most closely investigated in PD, as this disorder is well characterised both clinically and pathologically. PD is associated with a significant increase in iron in the degenerating substantia nigra (SN) and is measureable in living PD patients and in post-mortem brain. This increase, however, occurs only in the advanced stages of the disease, suggesting that this phenonoma may be a secondary, rather than a primary initiating event, a hypothesis also supported by evidence from animal experiments. The source of the increased iron is unknown but a variety of changes in iron homeostasis have been identified in PD, both in the brain and in the periphery. The possibility that an increased amount of iron may be transported into the SN is supported by data demonstrating that one form of the iron-binding glycoprotein transferrin family, lactotransferrin, is increased in surviving neurons in the SN in the PD brain and that this change is associated with increased numbers of lactotransferrin receptors on neurons and microvessels in the parkinsonian SN. These changes could represent one mechanism by which iron might concentrate within the PD SN. Alternatively, the measured increased in iron might result from a redistribution of ferritin iron stores. Ferritin is located in glial cells while the degenerating neurons do not stain positive for ferritin. As free radicals are highly reactive, it is unlikely that glial-derived free radicals diffuse across the intracellular space in sufficent quantities to damage neuronal constituents. If intracellular iron release contributes to neuronal damage it seems more probable that an intraneuronal iron source is responsible for oxidant-mediated damage. Such a iron source is neuromelanin (NM), a dark-coloured pigment found in the dopaminergic neurons of the human SN. In the normal brain, NM has the ability to bind a variety of metals, including iron, and increased NM-bound iron is reported in the parkinsonian SN. The consequences of these phenomena for the cell have not yet been clarified. In the absence of significant quantities of iron NM can act as an antioxidant, in that it can interact with and inactivate free radicals. On the other hand, in the presence of iron NM appears to act as a proxidant, increasing the rate of free radical production and thus the oxidative load within the vulnerable neurons. Given that increased iron is only apparent in the advanced stages of the disease it is unlikely that NM is of importance for the primary aetiology of PD. A localised increase in tissue iron and its interaction with NM may be, however, important as a secondary mechanism by increasing the oxidative load on the cell, thereby driving neurodegeneration.

Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 6. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 July 2021.
All research outputs
#4,709,809
of 22,849,304 outputs
Outputs from Journal of neural transmission Supplementum
#14
of 99 outputs
Outputs of similar age
#10,450
of 107,808 outputs
Outputs of similar age from Journal of neural transmission Supplementum
#2
of 10 outputs
Altmetric has tracked 22,849,304 research outputs across all sources so far. Compared to these this one has done well and is in the 76th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 99 research outputs from this source. They receive a mean Attention Score of 4.1. This one has done well, scoring higher than 85% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 107,808 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 83% of its contemporaries.
We're also able to compare this research output to 10 others from the same source and published within six weeks on either side of this one. This one has scored higher than 8 of them.