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The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates
Wakabayashi K, Tanji K, Mori F, Takahashi H.. Neuropathology : official journal of the Japanese Society of Neuropathology, 2007-10-01
Topic: Brain proteins, microglia and lab models
The histological hallmark of Parkinson's disease (PD) is the presence of fibrillar aggregates called Lewy bodies (LBs). LB formation has been considered to be a marker for neuronal degeneration, because neuronal loss is found in the predilection sites for LBs. To date, more than 70 molecules have been identified in LBs, in which alpha-synuclein is a major constituent of LB fibrils. Alpha-synuclein immunohistochemistry reveals that diffuse cytoplasmic staining develops into pale bodies via compaction, and that LBs arise from the peripheral portion of pale bodies. This alpha-synuclein abnormality is found in 10% of pigmented neurons in the substantia nigra and more than 50% of those in the locus ceruleus in PD. Recent studies have suggested that oligomers and protofibrils of alpha-synuclein are cytotoxic, and that LBs may represent a cytoprotective mechanism in PD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wakabayashi, K., Tanji, K., Mori, F., & Takahashi, H. (2007). The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates. Neuropathology : official journal of the Japanese Society of Neuropathology. https://doi.org/10.1111/j.1440-1789.2007.00803.x
Vancouver
Wakabayashi K, Tanji K, Mori F, Takahashi H. The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates. Neuropathology : official journal of the Japanese Society of Neuropathology. 2007. doi:10.1111/j.1440-1789.2007.00803.x. PMID: 18018486.
BibTeX
@article{wakabayashi2007-18018486,
author = {Wakabayashi, K. and Tanji, K. and Mori, F. and Takahashi, H.},
title = {{The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates}},
journal = {Neuropathology : official journal of the Japanese Society of Neuropathology},
year = {2007},
doi = {10.1111/j.1440-1789.2007.00803.x},
pmid = {18018486},
url = {https://doi.org/10.1111/j.1440-1789.2007.00803.x}
}
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Key findings
- Recent studies have suggested that oligomers and protofibrils of alpha-synuclein are cytotoxic, and that LBs may represent a cytoprotective mechanism in PD.
Why it matters
This review describes how Lewy bodies form from alpha-synuclein in Parkinson's disease and notes that recent studies suggest alpha-synuclein oligomers and protofibrils are cytotoxic while Lewy bodies may be protective. It is a summary of existing findings, not a treatment, cure or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuropathology : official journal of the Japanese Society of Neuropathology) |
| Journal's citation record | 1 / 4 | Neuropathology: journal h-index 83 (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 | 2007 — within 20 year(s) of the newest study here |
| 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 517 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 24.6 citations a year over 21 year(s) since 2007 |
| Impact for its field and year | 4 / 6 | Cited 12.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 77 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Hitoshi Takahashi: h-index 103 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Niigata University: institution h-index 473 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18018486) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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