Evidence map›Paper›PMID 40269912›Full record

ReviewMolecular neurodegeneration2025

Research models to study lewy body dementia.

Suelen Lucio Boschen, Aarushi A Mukerjee, Ayman H Faroqi, Ben E Rabichow, John Fryer

Abstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

5 authors.

Suelen Lucio BoschenDepartment of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Rd, Jacksonville, FL, 32224, USA. souza.suelen@mayo.edu.ORCID 0000-0002-7694-920X
Aarushi A MukerjeeDepartment of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Rd, Jacksonville, FL, 32224, USA.
Ayman H FaroqiMayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, 200 First St. SW, Rochester, MN, 55905, USA.
Ben E RabichowMayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, 200 First St. SW, Rochester, MN, 55905, USA.
John FryerTranslational Genomics Research Institute, 445 N 5th St, Phoenix, AZ, 850054, USA.

Funding

Modeling Lewy body dementia in vivo: Towards a better understanding of alpha synuclein and Tau interaction in diseaseR03NS112611 · NINDS · MAYO CLINIC JACKSONVILLE · PI DELENCLOS, MARION · 2020 to 2020
$157k
Fink Family Career Development Award in Neurology Fink Family Career Development Award in NeurologyFlorida Department of Health 20A07NIH/NIA R03NS112611NINDS NIH HHS R03 NS112611
6 · The paper itself

Abstract

Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. Clinical differentiation of LBD from Alzheimer's disease (AD) remains complex due to symptom overlap, yet approximately 25% of dementia cases are diagnosed as LBD postmortem, primarily identified by the presence of α-synuclein aggregates, tau tangles, and amyloid plaques. These pathological features position LBD as a comorbid condition of both Parkinson's disease (PD) and AD, with over 50% of LBD cases exhibiting co-pathologies. LBD's mixed pathology complicates the development of comprehensive models that reflect the full spectrum of LBD's etiological, clinical, and pathological features. While existing animal and cellular models have facilitated significant discoveries in PD and AD research, they lack specificity in capturing LBD's unique pathogenic mechanisms, limiting the exploration of therapeutic avenues for LBD specifically. This review assesses widely used PD and AD models in terms of their relevance to LBD, particularly focusing on their ability to replicate human disease pathology and assess treatment efficacy. Furthermore, we discuss potential modifications to these models to advance the understanding of LBD mechanisms and propose innovative research directions aimed at developing models with enhanced etiological, face, predictive, and construct validity.

Indexed as

Disease Models, AnimalLewy Body DiseaseParkinson Diseasealpha-SynucleinAlzheimer DiseaseAnimalsHumansalpha-SynucleinAlpha-synucleinAnimal modelBeta-amyloidCell cultureDementia with lewy bodyParkinson’s disease dementiaSynucleinopathyTau

Identifiers

PMID40269912
PMCPMC12020038

What OpenQuestion holds

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Registered trials

None linked

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.