The immune response within Alzheimer's disease: from the lense of peripheral monocyte-derived macrophages.

Hannah LeVasseur, Beiyan Zhou

Abstract readReview

In one paragraph

Review in Journal of neuroimmunology, 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

2 authors.

Hannah LeVasseurDepartment of Immunology, School of Medicine, University of Connecticut, Farmington, CT, USA.

Beiyan ZhouDepartment of Immunology, School of Medicine, University of Connecticut, Farmington, CT, USA; Institute for Systems Genomics, University of Connecticut, Farmington, CT, USA. Electronic address: bzhou@uchc.edu.

Funding

MiR-150 regulated adiose tissue B cells in obesityR01DK121805 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI VELLA, ANTHONY T, ZHOU, BEIYAN · 2020 to 2024

$2.0M

ASCVD risk assessment in T2DM facilitated by novel computational immunology programsR01HL172239 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI Anthony T Vella, Beiyan Zhou · 2024 to 2026

$1.6M

NHLBI NIH HHS R01 HL172239NIDDK NIH HHS R01 DK121805

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most significant form of dementia characterized by neurodegeneration and higher-order cognitive decline affecting over 6.9 million Americans age 65 and older. Emerging evidence for AD pathogenesis has expanded mechanistic investigation from focusing on the central nervous system (CNS), to including the peripheral immune system. Microglia in CNS and their counterpart peripheral monocyte-derived macrophages (MDMs) share fundamental functions as innate cells that contribute to the inflammatory response, phagocytosis of debris, and tissue repair after injury. As recently recognized in AD pathogenesis, MDMs have distinct origins and respond differently to environmental cues relative to microglia, presenting unique potentials for therapeutic targeting outside of the blood-brain barrier. In this review, we will diverge from the previously highlighted primary immune regulator in the CNS, the microglia, to explore the significance of MDMs as a peripheral-origin contributor to the pathogenesis of AD.

Indexed as

Alzheimer DiseaseMacrophagesMonocytesAnimalsHumansMicrogliaAlzheimer's diseaseInflammationMicrogliaMonocyte-derived macrophagesNeurodegeneration

Identifiers

PMID40753761

DOI10.1016/j.jneuroim.2025.578711

PMCPMC12904994

What OpenQuestion holds

Textmetadata

LicenceTDM

Read underepoch 390

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.