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The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia
Schulz-Schaeffer WJ.. Acta neuropathologica, 2010-06-20
Topic: Brain proteins, microglia and lab models
Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are usually associated with loss of dopaminergic neurons. Loss of substantia nigra neurons and presence of Lewy body inclusions in some of the remaining neurons are the hallmark pathology seen in the final stages of the disease. Attempts to correlate Lewy body pathology to either cell death or severity of clinical symptoms, however, have not been successful. While the pathophysiology of the neurodegenerative process can hardly be explained by Lewy bodies, the clinical symptoms do indicate a degenerative process located at the presynapse resulting in a neurotransmitter deficiency. Recently it was shown that 90% or even more of alpha-synuclein aggregates in DLB cases were located at the presynapses in the form of very small deposits. In parallel, dendritic spines are retracted, whereas the presynapses are relatively preserved, suggesting a neurotransmitter deprivation. The same alpha-synuclein pathology can be demonstrated for PD. These findings give rise to the notion that not cell death but rather alpha-synuclein aggregate-related synaptic dysfunction causes the neurodegeneration. This opens new perspectives for understanding PD and DLB. If presynaptic alpha-synuclein aggregation, not neuronal loss, is the key issue of the neurodegenerative process, then PD and DLB may eventually be treatable in the future. The disease may progress via trans-synaptical spread, suggesting that stem cell transplants are of limited use. Future therapies may focus on the regeneration of synapses.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Schulz-Schaeffer, W. J. (2010). The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia. Acta neuropathologica. https://doi.org/10.1007/s00401-010-0711-0
Vancouver
Schulz-Schaeffer WJ. The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia. Acta neuropathologica. 2010. doi:10.1007/s00401-010-0711-0. PMID: 20563819.
BibTeX
@article{schulzschaeffer2010-20563819,
author = {Schulz-Schaeffer, W. J.},
title = {{The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia}},
journal = {Acta neuropathologica},
year = {2010},
doi = {10.1007/s00401-010-0711-0},
pmid = {20563819},
url = {https://doi.org/10.1007/s00401-010-0711-0}
}
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.
Key findings
- Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are usually associated with loss of dopaminergic neurons.
- Recently it was shown that 90% or even more of alpha-synuclein aggregates in DLB cases were located at the presynapses in the form of very small deposits.
- The same alpha-synuclein pathology can be demonstrated for PD.
- These findings give rise to the notion that not cell death but rather alpha-synuclein aggregate-related synaptic dysfunction causes the neurodegeneration.
- The disease may progress via trans-synaptical spread, suggesting that stem cell transplants are of limited use.
Why it matters
This review argues that in Parkinson's disease and dementia with Lewy bodies, alpha-synuclein aggregates are mostly at presynapses and that synaptic dysfunction rather than cell death may cause symptoms. It raises the possibility that these diseases may eventually be treatable but reports no treatment tested in patients.
Study details
- Evidence strengthLow
How this study scored 53/100
Published in a leading specialty 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 | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 2010 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 625 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 34.7 citations a year over 18 year(s) since 2010 |
| Impact for its field and year | 4 / 6 | Cited 18.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 13 other studies in this library |
| Still being cited | 3 / 4 | Cited 133 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Walter Schulz‐Schaeffer: h-index 66 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Göttingen: institution h-index 934 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 20563819) |
| Free to read | 2 / 2 | Free to read |
| Total | 53 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s00401-010-0711-0
- PubMed: 20563819
- Original source →
- Free full text: Acta Neuropathologica →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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