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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Lewy body dementia

Topic: Brain proteins, microglia and lab models

Plain-language summary

Classic Parkinson's disease (PD) is characterized by fibrillar alpha-synuclein inclusions known as Lewy bodies in the substantia nigra, which are associated with nigrostriatal degeneration. However, alpha-synuclein pathologies accumulate throughout the CNS in areas that also undergo progressive neurodegeneration, leading to dementia and other behavioral impairments in addition to parkinsonism. Although mutations in the alpha-synuclein gene only cause Lewy body PD in rare families, and although there are multiple other, albeit rare, genetic causes of familial parkinsonism, sporadic Lewy body PD is the most common movement disorder, and insights into mechanisms underlying alpha-synuclein-mediated neurodegeneration provide novel targets for the discovery of disease-modifying therapies for PD and related neurodegenerative alpha-synucleinopathies.

What this study adds

Evidence grade: Low

This is a narrative review. This review describes how alpha-synuclein pathology in Parkinson's disease spreads through the brain and suggests that understanding these mechanisms could provide targets for disease-modifying therapies. It is a review, not a treatment, cure or prevention for Alzheimer's disease.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Lee, V. M., & Trojanowski, J. Q. (2006). Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery. Neuron. https://doi.org/10.1016/j.neuron.2006.09.026

Vancouver

Lee VM, Trojanowski JQ. Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery. Neuron. 2006. doi:10.1016/j.neuron.2006.09.026. PMID: 17015225.

BibTeX

@article{lee2006-17015225,
  author  = {Lee, V. M. and Trojanowski, J. Q.},
  title   = {{Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery}},
  journal = {Neuron},
  year    = {2006},
  doi     = {10.1016/j.neuron.2006.09.026},
  pmid    = {17015225},
  url     = {https://doi.org/10.1016/j.neuron.2006.09.026}
}

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

Why it matters

This review describes how alpha-synuclein pathology in Parkinson's disease spreads through the brain and suggests that understanding these mechanisms could provide targets for disease-modifying therapies. It is a review, not a treatment, cure or prevention for Alzheimer's disease.

Study details

How this study scored 49/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 4 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 4 of 6; Cited by studies here 2 of 6; Still being cited 2 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multicenter collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 49 of 100.49 of 100 points earned51 not earned

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.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neuron)
Journal's citation record 4 / 4 Neuron: journal h-index 689 (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 2006 — 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)
Randomized / blinded 0 / 2 No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 6 / 7 Cited 479 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 21.8 citations a year over 22 year(s) since 2006
Impact for its field and year 4 / 6 Cited 18.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 2 / 6 Cited by 7 other studies in this library
Still being cited 2 / 4 Cited 41 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)
Multicenter 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 17015225)
Free to read 0 / 2 Behind a paywall — scores zero
Total 49 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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