Evidence map›Paper›PMID 38815233›Full record

Observational studyNeurology2024

Differential Vulnerability of Hippocampal Subfields to Amyloid and Tau Deposition in the Lewy Body Diseases.

Rong Ye, Anna E Goodheart, Joseph J Locascio, Erin Peterec, Michael Properzi, Emma G Thibault, Erin Chuba, Keith A Johnson, Michael J Brickhouse, Alexandra Touroutoglou and 3 more

Abstract readObservational Study
In one paragraph

Observational study in Neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Regional cortical network atrophy predicts progression to dementia in the Lewy body diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  8. Article
  9. APOE ε4 linked effects on clinical features and neuropathology in dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  10. Plasma Phosphorylated Tau181 as a Biomarker for Alzheimer's Disease Co-Pathology in Lewy Body Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  11. Impact of hippocampal α-synuclein oligomers on cognitive trajectory in patients with dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  12. Article
  13. Article
  14. Cognitive Impact of β-Amyloid Load in the Rapid Eye Movement Sleep Behavior Disorder-Lewy Body Disease Continuum.Movement disorders : official journal of the Movement Disorder Society · 2024
    Article
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

13 authors.

Rong YeFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.
Anna E GoodheartFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.ORCID 0000-0001-8577-2090
Joseph J LocascioFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.
Erin PeterecFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.
Michael ProperziFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.ORCID 0000-0001-7855-2372
Emma G ThibaultFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.ORCID 0000-0002-7873-742X
Erin ChubaFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.
Keith A JohnsonFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.ORCID 0000-0002-5916-6043
Michael J BrickhouseFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.
Alexandra TouroutoglouFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.ORCID 0000-0001-9679-2433
John H GrowdonFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.
Bradford C DickersonFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.ORCID 0000-0002-5958-3445
Stephen N GompertsFrom the Department of Neurology (R.Y., A.E.G., J.J.L., E.P., M.P., E.G.T., E.C., K.A.J., M.J.B., A.T., J.G., B.C.D., S.N.G.), Massachusetts General Hospital, Boston; Mass General Institute of Neurodegenerative Disease (R.Y., A.E.G., E.P., S.N.G.), Charlestown; Lewy Body Dementia Unit (R.Y., A.E.G., E.P., S.N.G.) and Frontotemporal Disorders Unit (M.J.B., A.T., B.C.D.), Massachusetts General Hospital, Boston.

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
NIA NIH HHS P30 AG062421
6 · The paper itself

Abstract

BACKGROUND AND

objectivesAlzheimer disease (AD) copathologies of β-amyloid and tau are common in the Lewy body diseases (LBD), dementia with Lewy bodies (DLB) and Parkinson disease (PD), and target distinct hippocampal subfields compared with Lewy pathology, including subiculum and CA1. We investigated the hypothesis that AD copathologies impact the pattern of hippocampal subregion volume loss and cognitive function in LBD.

methodsThis was a cross-sectional and longitudinal, single-center, observational cohort study. Participants underwent neuropsychological testing and 3T-MRI with hippocampal segmentation using FreeSurferV7. PiB-PET and flortaucipir-PET imaging of comorbid β-amyloid (A) and tau (T) were acquired. The association of functional cognition, β-amyloid, and tau loads with hippocampal subregion volume was assessed. The contribution of subregion volumes to the relationship of AD-related deposits on functional cognition was examined with mediation analysis. The effects of AD-related deposits on the rate of subregion atrophy were evaluated with mixed-effects models.

resultsOf 103 participants (mean age: 70.3 years; 37.3% female), 52 had LBD with impaired cognition (LBD-I), 26 had normal cognition (LBD-N), and 25 were A- healthy controls (HCs). Volumes of hippocampal subregions prone to AD copathologies, including subiculum ( DISCUSSION: In LBD, volume loss in hippocampal output subregions-particularly the subiculum-is associated with functional cognition and AD-related deposits. Tau deposition appears to accelerate subiculum and CA1 atrophy, whereas Aβ does not. Subiculum volume may have value as a biomarker of AD copathology-mediated neurodegeneration and disease progression.

Indexed as

Amyloid beta-PeptidesHippocampusLewy Body DiseasePositron-Emission Tomographytau ProteinsAgedAged, 80 and overAlzheimer DiseaseCohort StudiesCross-Sectional StudiesFemaleHumansLongitudinal StudiesMagnetic Resonance ImagingMaleMiddle AgedAmyloid beta-Peptidestau Proteins

Identifiers

PMID38815233
PMCPMC11244748

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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.