Evidence map›Paper›PMID 40684248›Full record

ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Implications and opportunities regarding biological frameworks in overt and prodromal dementia with Lewy bodies.

Jennifer G Goldman, Bradley F Boeve, Douglas Galasko, John-Paul Taylor, James E Galvin, James B Leverenz, Frederic Blanc, Glenda Halliday, Kejal Kantarci, Afina W Lemstra and 10 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. 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. Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  2. Implications and opportunities regarding biological frameworks in overt and prodromal dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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

20 authors.

Jennifer G GoldmanMedical Division, JPG Enterprises LLC, Chicago, Illinois, USA.ORCID 0000-0001-5014-7535
Bradley F BoeveDepartment of Neurology and Center for Sleep Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Douglas GalaskoDepartment of Neurosciences, UC San Diego, La Jolla, California, USA.
John-Paul TaylorBiomedical Research Building, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, UK.
James E GalvinComprehensive Center for Brain Health, Department of Neurology, University of Miami Miller School of Medicine, Boca Raton, Florida, USA.
James B LeverenzDepartment of Neurology, VA-Puget Sound Health Care System, University of Washington, Seattle, Washington, USA.
Frederic BlancHdR, CM2R (Centre de Mémoire Ressources Et Recherche), Service de Gérontologie Mobile-Neuro-Psy-Recherche, GeRMINED Department, University Hospital of Strasbourg, and ICube Laboratory UMR-7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), IMIS Team, University of Strasbourg and CNRS, Strasbourg, France.
Glenda HallidayParkinson's Disease Research Clinic, Macquarie University Faculty of Medicine and Health Sciences, Sydney, New South Wales, Australia.
Kejal KantarciDepartment of Radiology, Division of Neuroradiology, Mayo Clinic, Rochester, Minnesota, USA.
Afina W LemstraAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, Amsterdam, the Netherlands.
Iracema LeroiGlobal Brain Health Institute and School of Medicine, Trinity College Dublin, College Green, Dublin, Ireland.
Simon J G LewisParkinson's Disease Research Clinic, Macquarie Medical School, Macquarie University, Sydney, New South Wales, Australia.
Irene LitvanDepartment of Neurosciences, Parkinson and Other Movement Disorders Center, UC San Diego, La Jolla, California, USA.
Helen MedsgerNorth Bay Lewy Body Dementia Caregiver Support Group, Santa Rosa, California, USA.
John O'BrienDepartment of Psychiatry, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Sonja W ScholzNeurodegenerative Diseases Research Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA.
Dag AarslandOld Age Psychiatry Department, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Manabu IkedaDepartment of Psychiatry, Osaka University Graduate School of Medicine, Osaka, Japan.
Ian McKeithBiomedical Research Building, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, UK.
Angela TaylorLewy Body Dementia Association, Atlanta, Georgia, USA.

Funding

UCSD Shiley-Marcos Alzheimer's Disease Research Center P30P30AG062429 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DOUGLAS R GALASKO · 2019 to 2026
$34.9M
Longitudinal Imaging Biomarkers of Prodromal DLBU01NS100620 · NINDS · MAYO CLINIC ROCHESTER · PI Bradley F Boeve, KEJAL KANTARCI · 2017 to 2026
$19.2M
Lewy Body Dementia AssociationNIA NIH HHS P30 AG062429NINDS NIH HHS U01 NS100620
6 · The paper itself

Abstract

Dementia with Lewy bodies (DLB), a progressive neurodegenerative disease with heterogeneous clinical presentations, greatly impacts patients, caregivers, and society. Despite its frequency, diagnosing and treating DLB remains challenging. Advances in in vivo biomarker assays reflecting underlying pathology are improving disease identification, diagnostic accuracy, and therapeutic development for biologically targeted, disease-modifying agents. Consequently, definitions of Alzheimer's disease and Parkinson's disease (PD) have shifted to focus on pathological changes occurring before clinical features, with proposed frameworks for detecting pathological amyloid and tau, neurodegeneration, and other markers (National Institute on Aging-Alzheimer's Association) and alpha-synucleinopathy and dopaminergic degeneration (Neuronal α-synuclein Disease Integrated Staging System, SynNeurGe). The biological frameworks, particularly those related to alpha-synuclein (α-synuclein), have sparked debate about unifying DLB and PD under a single pathobiologic disease. This paper discusses the implications of these biological frameworks for the DLB community, addressing topics regarding multiple pathologies and neurochemical systems, clinical heterogeneity, and functional impairment, and exploring the potential impact on clinical trials and care. HIGHLIGHTS: DLB is a progressive neurodegenerative disease with varied clinical presentations. Diagnosing and treating DLB remains challenging despite its frequency. Biological frameworks are reshaping Alzheimer's and Parkinson's definitions. In vivo biomarkers are improving DLB identification and diagnostic accuracy. Debate exists regarding unifying DLB and Parkinson's under one pathobiology.

Indexed as

Lewy Body DiseaseProdromal Symptomsalpha-SynucleinBiomarkersHumansParkinson Diseasealpha-SynucleinBiomarkersamyloidbiomarkerscognitive impairmentLewy body dementiaParkinsonismParkinson's disease dementiaprodromalsynuclein

Identifiers

PMID40684248
PMCPMC12276075

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.