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Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies
Irwin DJ, Lee VM, Trojanowski JQ.. Nature reviews. Neuroscience, 2013-07-31
Topic: Amyloid, tau and blood-test diagnosis
Dementia is increasingly being recognized in cases of Parkinson's disease (PD); such cases are termed PD dementia (PDD). The spread of fibrillar α-synuclein (α-syn) pathology from the brainstem to limbic and neocortical structures seems to be the strongest neuropathological correlate of emerging dementia in PD. In addition, up to 50% of patients with PDD also develop sufficient numbers of amyloid-β plaques and tau-containing neurofibrillary tangles for a secondary diagnosis of Alzheimer's disease, and these pathologies may act synergistically with α-syn pathology to confer a worse prognosis. An understanding of the relationships between these three distinct pathologies and their resultant clinical phenotypes is crucial for the development of effective disease-modifying treatments for PD and PDD.
Key findings
- Dementia is increasingly being recognized in cases of Parkinson's disease (PD); such cases are termed PD dementia (PDD).
- The spread of fibrillar α-synuclein (α-syn) pathology from the brainstem to limbic and neocortical structures seems to be the strongest neuropathological correlate of emerging dementia in PD.
- In addition, up to 50% of patients with PDD also develop sufficient numbers of amyloid-β plaques and tau-containing neurofibrillary tangles for a secondary diagnosis of Alzheimer's disease, and these pathologies may act synergistically with α-syn pathology to confer a worse prognosis.
- An understanding of the relationships between these three distinct pathologies and their resultant clinical phenotypes is crucial for the development of effective disease-modifying treatments for PD and PDD.
Why it matters
This review describes how the spread of alpha-synuclein pathology relates to dementia in Parkinson's disease, and notes that up to 50% of patients with Parkinson's disease dementia also develop amyloid-beta plaques and tau tangles sufficient for a secondary Alzheimer's disease diagnosis. It states that understanding these relationships is crucial for developing effective disease-modifying treatments, but reports no treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 54/100
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 (Nature reviews. Neuroscience) |
| Journal's citation record | 4 / 4 | Nature reviews. Neuroscience: journal h-index 572 (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 | 2013 — 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 872 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 58.1 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 3 / 6 | Cited 6.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 37 other studies in this library |
| Still being cited | 4 / 4 | Cited 209 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author John Q. Trojanowski: h-index 255 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Pennsylvania: institution h-index 1,859 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23900411) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 54 / 100 | — |
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Irwin, D. J., Lee, V. M., & Trojanowski, J. Q. (2013). Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies. Nature reviews. Neuroscience. https://doi.org/10.1038/nrn3549
Vancouver
Irwin DJ, Lee VM, Trojanowski JQ. Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies. Nature reviews. Neuroscience. 2013. doi:10.1038/nrn3549. PMID: 23900411.
BibTeX
@article{irwin2013-23900411,
author = {Irwin, D. J. and Lee, V. M. and Trojanowski, J. Q.},
title = {{Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies}},
journal = {Nature reviews. Neuroscience},
year = {2013},
doi = {10.1038/nrn3549},
pmid = {23900411},
url = {https://doi.org/10.1038/nrn3549}
}
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