Evidence map›Paper›PMID 35668160›Full record

ReviewMolecular psychiatry2022

Neuroimmune contributions to Alzheimer's disease: a focus on human data.

Verena Haage, Philip L De Jager

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.4field-weighted citation impact, top 4% 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.

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

57 citing papers in PubMed, 71 citations in OpenAlex.

  1. "Brain-IT": Exergame training with biofeedback breathing in neurocognitive disorders.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Trial
  2. Article
  3. Article
  4. Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Interleukin-6, CD8Frontiers in aging neuroscience · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Unraveling the oral microbiome's role in Alzheimer's disease: From pathophysiology to therapeutic potential.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Verena HaageCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-7569-8421
Philip L De JagerCenter for Translational & Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY, USA. pld2115@cumc.columbia.edu.ORCID http://orcid.org/0000-0002-8057-2505
Columbia University · USColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The past decade has seen the convergence of a series of new insights that arose from genetic and systems analyses of Alzheimer's disease (AD) with a wealth of epidemiological data from a variety of fields; this resulted in renewed interest in immune responses as important, potentially causal components of AD. Here, we focus primarily on a review of human data which has recently yielded a set of robust, reproducible results that exist in a much larger universe of conflicting reports stemming from small studies with important limitations in their study design. Thus, we are at an important crossroads in efforts to first understand at which step of the long, multiphasic course of AD a given immune response may play a causal role and then modulate this response to slow or block the pathophysiology of AD. We have a wealth of new experimental tools, analysis methods, and capacity to sample human participants at large scale longitudinally; these resources, when coupled to a foundation of reproducible results and novel study designs, will enable us to monitor human immune function in the CNS at the level of complexity that is required while simultaneously capturing the state of the peripheral immune system. This integration of peripheral and central perturbations in immune responses results in pathologic responses in the central nervous system parenchyma where specialized cellular microenvironments composed of multiple cell subtypes respond to these immune perturbations as well as to environmental exposures, comorbidities and the impact of the advancing life course. Here, we offer an overview that seeks to illustrate the large number of interconnecting factors that ultimately yield the neuroimmune component of AD.

Indexed as

Alzheimer DiseaseCausalityCentral Nervous SystemHumansResearch Design

Identifiers

PMID35668160
PMCPMC9168642
OpenAlexW4281735954

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.