Evidence map›Paper›PMID 36703235›Full record

ReviewGenome medicine2023

The neuroimmune axis of Alzheimer's disease.

Mehdi Jorfi, Anna Maaser-Hecker, Rudolph E Tanzi

Open access · goldAbstract readReview
In one paragraph

Review in Genome medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 3 pooled it
32.8field-weighted citation impact, top 1% 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

189 citing papers in PubMed, 3 syntheses or guidelines pooled it, 265 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Therapeutic Effects ofMolecules (Basel, Switzerland) · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Early microglial response to amyloid plaques drives sleep loss in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  17. Article
  18. Alzheimer's disease biological domain sub-stratification enhances the precision of functional analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  19. Article
  20. Article

129 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Mehdi JorfiGenetics and Aging Research Unit, Department of Neurology, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA. mjorfi@mgh.harvard.edu.
Anna Maaser-HeckerGenetics and Aging Research Unit, Department of Neurology, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA.
Rudolph E TanziGenetics and Aging Research Unit, Department of Neurology, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA. tanzi@helix.mgh.harvard.edu.
Harvard University · USMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a genetically complex and heterogeneous disorder with multifaceted neuropathological features, including β-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Over the past decade, emerging evidence has implicated both beneficial and pathological roles for innate immune genes and immune cells, including peripheral immune cells such as T cells, which can infiltrate the brain and either ameliorate or exacerbate AD neuropathogenesis. These findings support a neuroimmune axis of AD, in which the interplay of adaptive and innate immune systems inside and outside the brain critically impacts the etiology and pathogenesis of AD. In this review, we discuss the complexities of AD neuropathology at the levels of genetics and cellular physiology, highlighting immune signaling pathways and genes associated with AD risk and interactions among both innate and adaptive immune cells in the AD brain. We emphasize the role of peripheral immune cells in AD and the mechanisms by which immune cells, such as T cells and monocytes, influence AD neuropathology, including microglial clearance of amyloid-β peptide, the key component of β-amyloid plaque cores, pro-inflammatory and cytotoxic activity of microglia, astrogliosis, and their interactions with the brain vasculature. Finally, we review the challenges and outlook for establishing immune-based therapies for treating and preventing AD.

Indexed as

Alzheimer DiseaseNervous System DiseasesAmyloid beta-PeptidesBrainHumansMicrogliaNeuroimmunomodulationAmyloid beta-PeptidesAlzheimer’s diseaseHeterogeneityImmune systemNeuroimmuneβ-amyloid

Identifiers

PMID36703235
PMCPMC9878767
OpenAlexW4318067131

What Socratic holds

Textmetadata
LicenceCC BY
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.