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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 57 out of 100. Getting a diagnosis

Topic: Amyloid, tau and blood-test diagnosis

Objective A study was undertaken to examine the neuropathological substrates of cognitive dysfunction and dementia in Parkinson disease (PD). Methods One hundred forty patients with a clinical diagnosis of PD and either normal cognition or onset of dementia 2 or more years after motor symptoms (PDD) were studied. Patients with a clinical diagnosis of dementia with Lewy bodies were excluded. Autopsy records of genetic data and semiquantitative scores for the burden of neurofibrillary tangles, senile plaques, Lewy bodies (LBs), and Lewy neurites (LNs) and other pathologies were used to develop a multivariate logistic regression model to determine the independent association of these variables with dementia. Correlates of comorbid Alzheimer disease (AD) were also examined. Results Niney-two PD patients developed dementia, and 48 remained cognitively normal. Severity of cortical LB (CLB)/LN pathology was positively associated with dementia (p Interpretation CLB/LN pathology is the most significant correlate of dementia in PD. Additionally, APOE4 genotype may independently influence the risk of dementia in PD. AD pathology was abundant in a subset of patients, and may modify the clinical phenotype. Thus, therapies that target α-synuclein, tau, or amyloid β could potentially improve cognitive performance in PD.

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

APA 7th

Irwin, D. J., White, M. T., Toledo, J. B., Xie, S. X., Robinson, J. L., Van Deerlin, V., et al. (2012). Neuropathologic substrates of Parkinson disease dementia. Annals of neurology. https://doi.org/10.1002/ana.23659

Vancouver

Irwin DJ, White MT, Toledo JB, Xie SX, Robinson JL, Van Deerlin V, et al. Neuropathologic substrates of Parkinson disease dementia. Annals of neurology. 2012. doi:10.1002/ana.23659. PMID: 23037886.

BibTeX

@article{irwin2012-23037886,
  author  = {Irwin, D. J. and White, M. T. and Toledo, J. B. and Xie, S. X. and Robinson, J. L. and Van Deerlin, V. and Lee, V. M. and Leverenz, J. B. and others},
  title   = {{Neuropathologic substrates of Parkinson disease dementia}},
  journal = {Annals of neurology},
  year    = {2012},
  doi     = {10.1002/ana.23659},
  pmid    = {23037886},
  url     = {https://doi.org/10.1002/ana.23659}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Why it matters

This 2012 study examined the brains of 140 people with Parkinson disease after death: 92 had developed dementia and 48 had stayed cognitively normal. Clumps of the protein α-synuclein (Lewy bodies and Lewy neurites) in the brain's outer layer, the cortex, were "the most significant correlate of dementia". The gene variant APOE4 "may independently influence the risk", and Alzheimer-type changes were "abundant in a subset of patients". This is an association found at autopsy, not proof of cause. The authors' suggestion that therapies aimed at these proteins "could potentially" help thinking was not tested in this study.

Study details

How this study scored 57/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 3 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; Randomised / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 5 of 6; Cited by studies here 4 of 6; Still being cited 3 of 4; Senior author's track record 4 of 4; Institution's track record 3 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 57 of 100.57 of 100 points earned43 not earned

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.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (Annals of neurology)
Journal's citation record 3 / 4 Annals of Neurology: journal h-index 437 (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 2012 — 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 521 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 32.6 citations a year over 16 year(s) since 2012
Impact for its field and year 5 / 6 Cited 21.4× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 4 / 6 Cited by 44 other studies in this library
Still being cited 3 / 4 Cited 84 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 3 / 3 University of Washington: institution h-index 3,540 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 5 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 23037886)
Free to read 0 / 2 Behind a paywall — scores zero
Total 57 / 100 —

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