Cited by 693Parkinson's Disease Mechanisms and TreatmentsNeurological disorders and treatmentsNuclear Receptors and Signaling

Pathoanatomy of Parkinson’s disease

Braak, H., Braak, E.·2000·Journal of Neurology

Abstract

Parkinson's disease is a widespread degenerative illness affecting the human central, peripheral, and enteric nervous systems. The underlying pathological process progresses slowly but relentlessly and involves multiple neuronal systems. The disease is the consequence of changes in the neuronal cytoskeleton developing in only a few susceptible types of nerve cells. Afflicted neurons eventually produce Lewy bodies in their perikarya and Lewy neurites in their neuronal processes. Immunoreactions against the presynaptic protein alpha-synuclein have revealed many kinds of inclusion bodies ranging from inconspicuous dot- or thread-like forms to particularly voluminous types. The selective vulnerability of nerve cells induces a distinctive distribution pattern of lesions which remains remarkably consistent across cases. Components of the limbic system and the motor system have been shown to be particularly vulnerable to severe destruction. Some subnuclei of the substantia nigra also undergo major changes. This damage is consistently accompanied by extranigral alterations, with predilection sites including the entorhinal region, the second sector of the Ammon's horn, and important subnuclei of the amygdala. In addition, the nucleus of the stria terminalis, components of the hypothalamus, all of the non-thalamic nuclei with diffuse projections to the cerebral cortex, and most of the centers regulating autonomic functions exhibit severe lesions.

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Crossref · 10.1007/pl00007758

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  • Glutamatergic, cholinergic, GABA-ergic, tryptaminergic, noradrenergic and adrenergic nerve cells may show similar damage in their cytoskeleton in Parkinson's disease.

    “but glutamatergic, cholinergic, GABA-ergic, tryptaminergic, noradrenergic and adrenergic nerve cells may show similar damage in their cytoskeleton (Braak and Braak 2000).”

    From The clinical symptoms of Parkinson's disease. (2016) · cites this paper as Braak and Braak 2000

  • Degeneration of dopaminergic nigrostriatal neurons with Lewy bodies is regarded as the primary neuropathological correlate of motor impairment in Parkinson's disease.

    “The degeneration of dopaminergic nigrostriatal neurons with Lewy bodies is regarded as the primary neuropathological correlate of motor impairment in Parkinson's disease, but glutamatergic, cholinergic, GABA-ergic, tryptaminergic, noradrenergic and adrenergic nerve cells may show similar damage in their cytoskeleton (Braak and Braak 2000).”

    From The clinical symptoms of Parkinson's disease. (2016) · cites this paper as Braak and Braak 2000

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Authors
Braak, H., & Braak, E.
Affiliations
Goethe University Frankfurt (DE)
Venue
Journal of Neurology
Published
2000-04-10
Volume
247
Issue
S2
Pages
II3-II10
ISSN
  • 0012-1037 (ISSN-L)
  • 0340-5354
OpenAlex
W2081355012
Cited by
693
References
4
Citations by year
2026: 15 · 2025: 31 · 2024: 31 · 2023: 25 · 2022: 34 · 2021: 35 · 2020: 33 · 2019: 30 · 2018: 24 · 2017: 33 · 2016: 32 · 2015: 22 · 2014: 32 · 2013: 41 · 2012: 28
FWCI
12.15
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Deutsche Forschungsgemeinschaft
  • Bundesministerium für Forschung und Technologie
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Neurology › Neurological disorders and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
Parkinson's disease, pathological anatomy, Lewy bodies, Lewy neurites, alpha-synuclein, neuronal cytoskeleton, neuronal vulnerability, substantia nigra, limbic system, amygdala, entorhinal cortex, stria terminalis, hypothalamus, autonomic nervous system, neurodegeneration
MeSH terms
Brain, Humans, Neural Pathways, Parkinson Disease

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