Evidence map›Paper›PMID 38795783›Full record

ArticleBrain, behavior, and immunity2024

Evidence for reduced anti-inflammatory microglial phagocytic response in late-life major depression.

Chelsea Reichert Plaska, Amanda Heslegrave, Davide Bruno, Jaime Ramos-Cejudo, Sang Han Lee, Ricardo Osorio, Bruno P Imbimbo, Henrik Zetterberg, Kaj Blennow, Nunzio Pomara

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain, behavior, and immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. 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

10 authors.

Chelsea Reichert PlaskaGeriatric Psychiatry Division, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Psychiatry, New York University Grossman School of Medicine, New York, NY, USA.
Amanda HeslegraveDepartment of Neurodegenerative Disease, UCL Institute of Neurology, London, United Kingdom; UK Dementia Research Institute at UCL, London, United Kingdom.
Davide BrunoSchool of Psychology, Liverpool John Moores University, Liverpool, United Kingdom.
Jaime Ramos-CejudoDepartment of Psychiatry, New York University Grossman School of Medicine, New York, NY, USA; VA Boston Cooperative Studies Program MAVERIC, VA Boston Healthcare System, Boston, MA, USA.
Sang Han LeeGeriatric Psychiatry Division, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Psychiatry, New York University Grossman School of Medicine, New York, NY, USA.
Ricardo OsorioDepartment of Psychiatry, New York University Grossman School of Medicine, New York, NY, USA; Clinical Research Department, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY, USA.
Bruno P ImbimboDepartment of Research & Development, Chiesi Farmaceutici, Parma, Italy.
Henrik ZetterbergDepartment of Neurodegenerative Disease, UCL Institute of Neurology, London, United Kingdom; UK Dementia Research Institute at UCL, London, United Kingdom; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China; Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Paris Brain Institute, ICM, Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France; Neurodegenerative Disorder Research Center, Division of Life Sciences and Medicine, and Department of Neurology, Institute on Aging and Brain Disorders, University of Science and Technology of China and First Affiliated Hospital of USTC, Hefei, P.R. China.
Nunzio PomaraGeriatric Psychiatry Division, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Psychiatry and Pathology, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: nunzio.pomara@nki.rfmh.org.

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
Slow wave sleep (SWS) and the effect of African ancestry on amyloid burden, a longitudinal studyR01AG056531 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI JEAN-LOUIS, GIRARDIN, OSORIO, RICARDO S · 2018 to 2022
$6.7M
Promoting Academic Workforce Development in Behavioral Medicine and Sleep Disorders ResearchR25HL105444 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Girardin Jean-Louis, Tatjana Rundek · 2010 to 2026
$5.8M
Sleep Aging and Risk for Alzheimer's disease-Resubmission-1R01AG056031 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI OSORIO, RICARDO S · 2018 to 2022
$4.4M
Depression treatment and Aβ dynamics: A study of Alzheimer’s disease riskR01AG070821 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI POMARA, NUNZIO · 2021 to 2025
$3.9M
Plasma and CSF Abeta peptides in late-onset major depressionR01MH080405 · NIMH · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI POMARA, NUNZIO · 2007 to 2011
$1.6M
NHLBI NIH HHS R25 HL105444NIA NIH HHS P30 AG008051NIA NIH HHS R01 AG056031NIA NIH HHS R01 AG056531NIA NIH HHS R01 AG070821NIMH NIH HHS R01 MH080405
6 · The paper itself

Abstract

Major depressive disorder (MDD) is associated with Alzheimer's disease (AD) but the precise mechanisms underlying this relationship are not understood. While it is well established that cerebrospinal fluid (CSF) soluble levels of triggering receptor expressed on myeloid cells 2 (sTREM2) increase during early stages of AD, how sTREM2 levels behave in subjects with MDD is not known. In a longitudinal study, we measured CSF sTREM2 levels in 27 elderly cognitively intact individuals with late-life major depression (LLMD) and in 19 healthy controls. We tested the hypothesis that, similarly to what happens in early stages of AD, CSF sTREM2 would be elevated in MDD. In addition, we compared the associations of CSF sTREM2, pro- and anti- inflammatory, and AD biomarkers in LLMD and control subjects. Surprisingly, we found that mean CSF sTREM2 levels were significantly reduced in LLMD compared to controls. This reduction was no longer significant at the 3-year follow-up visit when depression severity improved. In addition, we found that CSF sTREM2 was associated with AD biomarkers and proinflammatory cytokines in controls but not in LLMD. These findings suggest that impaired microglia phagocytic response to AD pathology may be a novel link between MDD and AD.

Indexed as

Alzheimer DiseaseBiomarkersMajor Depressive DisorderMembrane GlycoproteinsMicrogliaReceptors, ImmunologicAgedAged, 80 and overCytokinesFemaleHumansInflammationLongitudinal StudiesMaleMiddle AgedPhagocytosisBiomarkersCytokinesMembrane GlycoproteinsReceptors, ImmunologicTREM2 protein, humanAlzheimer’s diseaseAmyloid betaDepressionMicrogliaPhagocytosissTREM2

Identifiers

PMID38795783
PMCPMC11270917

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Registered trials

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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.