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Cell death mechanisms in Parkinson's disease
Jellinger KA.. Journal of neural transmission (Vienna, Austria : 1996), 2000-01-01
Topic: Brain proteins, microglia and lab models
Objective While the causes of neuronal death in Parkinson's disease (PD) and other neurodegenerative disorders are still unknown, several mechanisms are under discussion: programmed vs. passive cell death (apoptosis vs. necrosis), mainly based on conflicting results on the rare presence or absence of DNA fragmentation in substantia nigra neurons using the in situ DNA-labeling (TUNEL) method. Design/methods In 4 cases of Parkinson's disease (PD), 2 cases of Dementia with Lewy bodies (DLB) and 3 age-matched controls, the TUNEL/ISEL method was used to detect DNA fragmentation in substantia nigra locus coeruleus and cerebral cortex [method by Gold et al. In addition, immunohistochemistry was performed for an array of apoptosis-related proteins, i.e. the recently described apoptosis specific protein cJun/AP1 (ASP), the proto-oncogenes c-Jun, c-Jun AP1, Bcl2, Bax, Bcl-x, p53, CD 95 (Fas/Apo-1)
Key findings
- Design/methods In 4 cases of Parkinson's disease (PD), 2 cases of Dementia with Lewy bodies (DLB) and 3 age-matched controls, the TUNEL/ISEL method was used to detect DNA fragmentation in substantia nigra locus coeruleus and cerebral cortex [method by Gold et al.
- In addition, immunohistochemistry was performed for an array of apoptosis-related proteins, i.e. the recently described apoptosis specific protein cJun/AP1 (ASP), the proto-oncogenes c-Jun, c-Jun AP1, Bcl2, Bax, Bcl-x, p53, CD 95 (Fas/Apo-1), activated caspase 3, several heat shock proteins (alpha-B crystallin, ubiquitin), and alpha-synuclein.
- Results None of the cases of PD, DLB, and controls showed convincing TUNEL-positivity nor morphologic signs of apoptosis in nigral, locus coeruleus or cortical neurons with or without Lewy bodies but variable numbers of TUNEL-positive astrocytes and microglial cells in substantia nigra of PD and DLB.
- There were no significant differences in the expression of c-Jun, ASP, Bcl-2, Bax, and Bcl-x in substantia nigra neurons between PD, DLB, and controls nor between cortical and subcortical neurons with and without Lewy bodies.
Why it matters
This study examined brain tissue from 4 people with Parkinson's disease, 2 with dementia with Lewy bodies and 3 age-matched controls for DNA fragmentation and apoptosis-related proteins. It addresses mechanisms of cell death in Parkinson's disease, not Alzheimer's disease, and the small number of cases limits what can be concluded.
Study details
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neural transmission (Vienna, Austria : 1996)) |
| Journal's citation record | 2 / 4 | Journal of Neural Transmission: journal h-index 167 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2000 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 227 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.1 citations a year over 28 year(s) since 2000 |
| Impact for its field and year | 4 / 6 | Cited 14.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author K. A. Jellinger: h-index 137 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Ludwig Boltzmann für Klinische Neurobiologie: institution h-index 82 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 10809400) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Jellinger, K. A. (2000). Cell death mechanisms in Parkinson's disease. Journal of neural transmission (Vienna, Austria : 1996). https://doi.org/10.1007/s007020050001
Vancouver
Jellinger KA. Cell death mechanisms in Parkinson's disease. Journal of neural transmission (Vienna, Austria : 1996). 2000. doi:10.1007/s007020050001. PMID: 10809400.
BibTeX
@article{jellinger2000-10809400,
author = {Jellinger, K. A.},
title = {{Cell death mechanisms in Parkinson's disease}},
journal = {Journal of neural transmission (Vienna, Austria : 1996)},
year = {2000},
doi = {10.1007/s007020050001},
pmid = {10809400},
url = {https://doi.org/10.1007/s007020050001}
}
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