Evidence map›Paper›PMID 37883190›Full record

ArticleThe Journal of clinical investigation2024

Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases.

David S Goldstein, Courtney Holmes, Patti Sullivan, Grisel Lopez, Janna Gelsomino, Sarah Moore, Risa Isonaka, Tianxia Wu, Yehonatan Sharabi

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00775853 (Biomarkers of Risk of Parkinson Disease), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
7.6field-weighted citation impact, top 2% of its field
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.

NCT00775853 completednot on this map

Biomarkers of Risk of Parkinson Disease

TypeobservationalSponsorNational Institute of Neurological Disorders and Stroke (NINDS)Ran2009 to 2023Enrolled89ConditionsParkinson Disease, Autonomic Nervous System Diseases, Pure Autonomic FailureArms6-[18F]Fluorodopamine, 6-[18F]Fluorodopa, 13N-Ammonia
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Preclinical Catecholaminergic Biomarkers of Central Lewy Body Diseases.Journal of clinical neurology (Seoul, Korea) · 2026
    Review
  4. Multitracer PET to Assess Cardiac Sympathetic Innervation and Vesicular Storage in Lewy Body Diseases.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
    Article
  5. 3,4-Dihydroxyphenylglycol levels separate multiple system atrophy from Parkinson disease with orthostatic hypotension.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
    Observational
  6. "Body-first" dementia with Lewy bodies.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
    Article
  7. Review
  8. Review
  9. Review
  10. 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
  11. Article
  12. Article
  13. Decreased urinary excretion of norepinephrine and dopamine in autonomic synucleinopathies.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
    Article
  14. Review
  15. Observational
  16. Article
  17. A pathophysiological biomarker combination separates Lewy body from non-Lewy body neurogenic orthostatic hypotension ​.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2024
    Observational
  18. Heart-brain axis: Pushing the boundaries of cardiovascular molecular imaging.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2024
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

David S GoldsteinAutonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS).
Courtney HolmesAutonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS).
Patti SullivanAutonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS).
Grisel LopezMolecular Neurogenetics Section, National Human Genome Research Institute, and.
Janna GelsominoAutonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS).
Sarah MooreAutonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS).
Risa IsonakaAutonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research (DIR), National Institute of Neurological Disorders and Stroke (NINDS).
Tianxia WuClinical Trials Unit, Office of the Clinical Director, DIR, NINDS, NIH, Bethesda, Maryland, USA.
Yehonatan SharabiChaim Sheba Medical Center, Tel-Aviv University, Tel-Hashomer, Israel.
National Institute of Neurological Disorders and Stroke · USNational Human Genome Research Institute · USOffice of the Director · USTel Aviv University · IL

Funding

Biomarkers of Parkinson Disease and Related DisordersZIANS003034 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI GOLDSTEIN, DAVID · 2009 to 2025
$22.8M
6 · The paper itself

Abstract

backgroundIn Lewy body diseases (LBDs) Parkinson disease (PD), and dementia with Lewy bodies (DLB), by the time parkinsonism or cognitive dysfunction manifests clinically, substantial neurodegeneration has already occurred. Biomarkers are needed to identify central LBDs in a preclinical phase, when neurorescue strategies might forestall symptomatic disease. This phase may involve catecholamine deficiency in the autonomic nervous system. We analyzed data from the prospective, observational, long-term PDRisk study to assess the predictive value of low versus normal cardiac 18F-dopamine positron emission tomography (PET), an index of myocardial content of the sympathetic neurotransmitter norepinephrine, in at-risk individuals.

methodsParticipants self-reported risk factor information (genetics, olfactory dysfunction, dream enactment behavior, and orthostatic intolerance or hypotension) at a protocol-specific website. Thirty-four with 3 or more confirmed risk factors underwent serial cardiac 18F-dopamine PET at 1.5-year intervals for up to 7.5 years or until PD was diagnosed.

resultsNine participants had low initial myocardial 18F-dopamine-derived radioactivity (<6,000 nCi-kg/cc-mCi) and 25 had normal radioactivity. At 7 years of follow-up, 8 of 9 with low initial radioactivity and 1 of 11 with normal radioactivity were diagnosed with a central LBD (LBD+) (P = 0.0009 by Fisher's exact test). Conversely, all 9 LBD+ participants had low 18F-dopamine-derived radioactivity before or at the time of diagnosis of a central LBD, whereas among 25 participants without a central LBD only 1 (4%) had persistently low radioactivity (P < 0.0001 by Fisher's exact test).

conclusionCardiac 18F-dopamine PET highly efficiently distinguishes at-risk individuals who are diagnosed subsequently with a central LBD from those who are not.

trial registrationCLINICALTRIALS: gov NCT00775853.

fundingDivision of Intramural Research, NIH, NINDS.

Indexed as

DopamineParkinson DiseaseHumansLewy BodiesNorepinephrinePositron-Emission TomographyProspective StudiesDopamineNorepinephrineNeurodegenerationNeuroimagingNeuroscienceParkinson disease

Identifiers

PMID37883190
PMCPMC10760969
OpenAlexW4387948480

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.