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Cited by 132Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsParkinson's Disease Mechanisms and Treatments

The DOI matches its Crossref record; 191 of the 193 references it cites were found in a registry or an index.

General aspects of neurodegeneration

Jellinger, K. A.·2003·Journal of Neural Transmission. Supplementa
DOI 10.1007/978-3-7091-0643-3_7
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Abstract

Neurodegenerative diseases are morphologically featured by progressive cell loss in specific vulnerable neuronal populations of the central nervous system, often associated with cytoskeletal protein aggregates forming intracytoplasmic and/or intranuclear inclusions in neurons and/or glial cells. Most neurodegenerative disorders are now classified either according to the hitherto known genetic mechanisms or to the major components of their cellular protein inclusions. The major basic processes inducing neurodegeneration are considered multifactorial ones caused by genetic, environmental, and endogenous factors. They include abnormal protein dynamics with defective protein degradation and aggregation, many of them related to the ubiquitin-proteasomal system, oxidative stress and free radical formation, impaired bioenergetics and mitochondrial dysfunctions, and "neuroinflammatory" processes. These mechanisms that are usually interrelated in complex vitious circles finally leading to programmed cell death cascades are briefly discussed with reference to their pathogenetic role in many, albeit diverse neurodegenerative diseases, like Alzheimer disease, synucleinopathies, tauopathies, and polyglutamine disorders. The impact of protein inclusions on cell dysfunction, activation or prevention of cell death cascades are discussed, but the molecular basis for the underlying disease mechanisms remains to be elucidated.

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Crossref · 10.1007/978-3-7091-0643-3_7

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2 of the 193 references couldn’t be matched to a known paper.

Research works printed but not linked: 19

  1. Bence NF, Sampat RM, Kopito RR (2001) Impairment of the ubiquitin-proteasome system by protein aggregation. Science 292: 1552–1555 · DOI
  2. Cluskey S, Ramsden DB (2001) Mechanisms of neurodegeneration in amyotrophic lateral sclerosis. Mol Pathol 54: 386–392
  3. Henry JM, Jellinger KA (2003) Postencephalitic parkinsonism. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
  4. Jellinger KA (2003b) Experimental models of synucleinopathies. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
  5. Jellinger KA, Duda J (2003) Neuroaxonal dystrophies. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
  6. Jellinger KA, Mizuno Y (2003) Parkinson disease. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
  7. Lantos PL, Quinn N (2003) Dementia with Lewy bodies. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
  8. Linert W, Jellinger KA (2001) Cell death mechanisms and the role of iron in neurodegeneration. In: Segura-Aquilar J (ed) Mechanisms of degeneration and protection of the dopaminergic system. FP Graham Publishing, Johnson City, pp 21–65
  9. Lippa CF (2003) Lewy bodies in conditions other than disorders of α-synuclein. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
  10. McGeer PL, McGeer EG (2002) Polymorphisms in inflammatory genes enhance the risk of Alzheimer disease. Alzheimer Research Forum, February 11, 2002
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  15. Perry G, Srinivas R, Nunomura A, Smith MA (2003) Oxidative mechanisms in neurodegenerative diseases. In: Dickson DW et al (eds) Neurodegeneration and dementias. ISN Neuropathology Press, Los Angeles (in press)
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  17. Simon DK, Beal MF (2002) Pathogenesis: oxidative stress, mitochondrial dysfunction and excitotoxicity. In: Factor SA, Weiner WJ (eds) Parkinson’s disease. Diagnosis and management. Demos, New York, pp 281–290
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Metadata

Authors
Jellinger, K. A.
Corresponding author
Jellinger, K. A.
ORCID
Jellinger, K. A.
Venue
Journal of Neural Transmission. Supplementa
Publisher
Springer Vienna
Published
2003
Issue
65
Pages
101-144
ISSN
0303-6995 (ISSN-L)
DOI
10.1007/978-3-7091-0643-3_7
OpenAlex
W48785815
Cited by
126
References
193
Citations by year
2025: 1 · 2024: 6 · 2023: 4 · 2022: 7 · 2021: 3 · 2020: 5 · 2019: 2 · 2018: 6 · 2017: 6 · 2016: 3 · 2015: 3 · 2014: 9 · 2013: 7 · 2012: 8
FWCI
39.40
Type
book chapter
Language
en
Open access
closed
Locations
  • Journal of neural transmission. Supplementum (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
neurodegeneration, neurodegenerative diseases, protein aggregation, protein inclusions, ubiquitin-proteasome system, oxidative stress, mitochondrial dysfunction, bioenergetics, neuroinflammation, programmed cell death, Alzheimer's disease, synucleinopathies, tauopathy, polyglutamine diseases, neuronal loss
MeSH terms
Animals, Inclusion Bodies, DNA, Mitochondrial, Humans, Iron, Mitochondria, Mutation, Nerve Degeneration, Nerve Tissue Proteins, Neuroglia, Neurons, Ubiquitins, Signal Transduction, Cell Death, Oxidative Stress, Neurodegenerative Diseases

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