Evidence map›Paper›PMID 39281742›Full record

ArticlemedRxiv : the preprint server for health sciences2024

Clinicopathological Heterogeneity of Lewy Body Diseases: The Profound Influence of Comorbid Alzheimer's Disease.

Thomas G Beach, Geidy E Serrano, Nan Zhang, Erika D Driver-Dunckley, Lucia I Sue, Holly A Shill, Shyamal H Mehta, Christine Belden, Cecilia Tremblay, Parichita Choudhury and 2 more

Abstract readPreprint
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Thomas G BeachBanner Sun Health Research Institute, Sun City, AZ.
Geidy E SerranoBanner Sun Health Research Institute, Sun City, AZ.ORCID 0000-0002-9527-2011
Nan ZhangMayo Clinic, Scottsdale, AZ.
Erika D Driver-DunckleyMayo Clinic, Scottsdale, AZ.
Lucia I SueBanner Sun Health Research Institute, Sun City, AZ.
Holly A ShillBarrow Neurological Institute, Phoenix, AZ.
Shyamal H MehtaMayo Clinic, Scottsdale, AZ.
Christine BeldenBanner Sun Health Research Institute, Sun City, AZ.
Cecilia TremblayBanner Sun Health Research Institute, Sun City, AZ.
Parichita ChoudhuryBanner Sun Health Research Institute, Sun City, AZ.
Alireza AtriBanner Sun Health Research Institute, Sun City, AZ.
Charles H AdlerMayo Clinic, Scottsdale, AZ.

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI REIMAN, ERIC MICHAEL · 2001 to 2020
$32.5M
Research Education ComponentP30AG072980 · NIA · BANNER HEALTH · PI Nicholas Ashton · 2021 to 2026
$24.9M
National Brain and Tissue Resource for Parkinson's Disease and Related DisordersU24NS072026 · NINDS · BANNER SUN HEALTH RESEARCH INSTITUTE · PI BEACH, THOMAS G · 2011 to 2015
$7.8M
NIA NIH HHS P30 AG019610NIA NIH HHS P30 AG072980NINDS NIH HHS U24 NS072026
6 · The paper itself

Abstract

In recent years, proposals have been advanced to redefine or reclassify Lewy body disorders by merging the long-established entities of Parkinson's disease (PD), Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB). These proposals reject the International DLB Consortium classification system that has evolved over three decades of consensus collaborations between neurologists, neuropsychologists and neuropathologists. While the Consortium's "one year rule" for separating PD and DLB has been criticized as arbitrary, it has been a pragmatic and effective tool for splitting the continuum between the two entities. In addition to the decades of literature supporting the non-homogeneity of PD and DLB, it has become increasingly apparent that Lewy body disorders may fundamentally differ in their etiology. Most PD subjects, as well as most clinically-presenting DLB subjects, might best be classified as having a "primary synucleinopathy" while most clinically-unidentified DLB subjects, who also have concurrent neuropathology-criteria AD (AD/DLB), as well as those with neuropathological AD and amygdala-predominant LBD insufficient for a DLB diagnosis, may best be classified as having a "secondary synucleinopathy. Importantly, the DLB Consortium recognized the importance of comorbid AD pathology by defining "Low", "Intermediate" and "High" subdivisions of DLB based on the relative brain stages of both Lewy body and AD pathology. If the one-year rule for separating PD from DLB, and for then dividing DLB into subtypes based on the presence and severity of comorbid AD pathology, is effective, then the divided groups should statistically differ in important ways. In this study we used the comprehensive clinicopathological database of the Arizona Study of Aging and Neurodegenerative Disorders (AZSAND) to empirically test this hypothesis. Furthermore, we used multivariable statistical models to test the hypothesis that comorbid AD neuropathology is a major predictor of the presence and severity of postmortem Lewy synucleinopathy. The results confirm the clinicopathological heterogeneity of Lewy body disorders as well as the profound influence of comorbid AD pathology.

Identifiers

PMID39281742
PMCPMC11398443

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.