Evidence map›Paper›PMID 41271423›Full record

ArticleBMJ open2025

Immune Profiling in Early Cognitive Disorders (IMPRINT) study protocol: a longitudinal cohort study exploring biomarkers of inflammation in early dementia with Lewy bodies and Alzheimer's disease, as part of the Dementias Platform UK.

Harry Crook, Peter Swann, Haddy Fye, Stacey Kigar, George Savulich, Anna Mckeever, Elena Herrero, Lordina Turner, Lina Aimola, Gabrielle D Grey and 7 more

Abstract read
In one paragraph

Article in BMJ open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Harry CrookDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-6206-470X
Peter SwannDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
Haddy FyeDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Stacey KigarDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
George SavulichDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
Anna MckeeverDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
Elena HerreroDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
Lordina TurnerDepartment of Medicine, University of Cambridge, Cambridge, England, UK.
Lina AimolaDepartment of Brain Sciences, Imperial College London, London, UK.
Gabrielle D GreyDepartment of Brain Sciences, Imperial College London, London, UK.
Dan BlackburnThe University of Sheffield, Sheffield, England, UK.
Paul M MatthewsDepartment of Brain Sciences, Imperial College London, London, UK.
Li SuDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
Leonidas ChouliarasDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK.
James B RoweDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Paresh MalhotraDepartment of Brain Sciences, Imperial College London, London, UK.
John T O'BrienDepartment of Psychiatry, University of Cambridge, Cambridge, England, UK john.obrien@medschl.cam.ac.uk.ORCID http://orcid.org/0000-0002-0837-5080

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGrowing evidence points towards the integral role of both central and peripheral inflammation across all neurodegenerative diseases, including dementia with Lewy bodies (DLB) and Alzheimer's disease (AD). The immune alterations observed in these diseases may occur long before the onset of clinical and cognitive symptoms; however, the exact timing and role of inflammation in the pathogenesis of neurodegenerative disease remains unclear. Findings to date are conflicting, with most work focused on AD rather than other dementias and most studies from single sites and cross-sectional. Through longitudinally examining detailed phenotypes of the peripheral immune system using mass cytometry, the Immune Profiling in Early Cognitive Disorders study aims to uncover specific immune signatures in early AD and DLB, how these signatures change over time and how they relate to disease progression and cognitive changes. METHODS AND ANALYSIS: Blood, cerebrospinal fluid, saliva and urine samples will be collected from a cohort of participants with either prodromal (mild cognitive impairment) or early dementia due to Lewy bodies or AD (MCI-LB and DLB; and MCI-AD and AD), alongside healthy controls. Through immunophenotyping with mass cytometry, detailed immune fingerprints will be identified for these groups. We will assess which key combinations of immune cell clusters are predictive of disease phenotype, cognitive decline and progression to dementia. Samples will also be evaluated with novel techniques to measure markers of degenerative pathology and inflammation. ETHICS AND DISSEMINATION: This study was approved by the Preston North West Research Ethics committee (21/NW/0314) and is registered with the ISRCTN registry (ISRCTN62392656). The study is ongoing (since June 2022). Baseline visits are being undertaken, and follow-up visits have started for some participants. Full data analyses will be completed and submitted for publication upon conclusion of the study.

Indexed as

Alzheimer DiseaseCognitive DysfunctionInflammationLewy Body DiseaseAgedBiomarkersDisease ProgressionFemaleHumansLongitudinal StudiesMaleUnited KingdomBiomarkersDementiaImmunophenotypingOld age psychiatry

Identifiers

PMID41271423
PMCPMC12658555

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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.