Evidence map›Paper›PMID 31440234›Full record

ReviewFrontiers in immunology2019

Is Innate Memory a Double-Edge Sword in Alzheimer's Disease? A Reappraisal of New Concepts and Old Data.

Francesca Salani, Valentina Sterbini, Eleonora Sacchinelli, Mariagrazia Garramone, Paola Bossù

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Elimination of senescent cells fails to attenuate disease progression in an ALS mouse model.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  2. Monocolonization withMicrobiology spectrum · 2026
    Article
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  9. MnTheranostics · 2025
    Article
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  18. Depression, dementia and immune dysregulation.Brain : a journal of neurology · 2021
    Article
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  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

5 authors.

Francesca SalaniExperimental Neuropsychobiology Lab, IRCCS Santa Lucia Foundation, Rome, Italy.
Valentina SterbiniExperimental Neuropsychobiology Lab, IRCCS Santa Lucia Foundation, Rome, Italy.
Eleonora SacchinelliExperimental Neuropsychobiology Lab, IRCCS Santa Lucia Foundation, Rome, Italy.
Mariagrazia GarramoneExperimental Neuropsychobiology Lab, IRCCS Santa Lucia Foundation, Rome, Italy.
Paola BossùExperimental Neuropsychobiology Lab, IRCCS Santa Lucia Foundation, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An emergent concept in immunology suggests that innate immune system is capable to undergo non-specific long-term responses and to provide resistance by modifying the reactivity to sequential pathogen challenge. This phenomenon, named innate memory, involves epigenetic, and metabolic reprogramming of innate immune cells. Current literature shows that the innate memory process has a mainly beneficial role in host defense, but sometimes can exert detrimental effects, as common in many diseases. Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and dementia. Accumulating findings demonstrate that inflammation is involved in AD pathogenesis and progression and recent genetic and functional data confirm the driving role of the innate immune component in the disease. Furthermore, AD patients show high burden of the most relevant infectious agents and up-regulation of inflammatory features in their innate immune cells, including an activated, or "primed" status of myeloid phagocytic cells in both brain and periphery, resembling trained immunity conditions. Thus, it is conceivable that AD innate cells may be firstly involved in the attempt to resolve recurrent/persistent inflammation but then acquire a trained phenotype mostly unable to maintain the immune regulation, leaving uncontrolled or sometimes supporting the progression of neurodegeneration. The present review aims to summarize evidence evoking innate immune memory mechanisms in AD, and to interpret their potential role, either protective or harmful, in disease progression. A better understanding of such mechanisms will provide a fertile ground for development of novel diagnostic, and therapeutic pathways in AD cure.

Indexed as

Immunity, InnateImmunologic MemoryAlzheimer DiseaseHumansInflammationAlzheimer's diseaseinnate immune cellstrained immunitytrained potentiationtrained tolerance

Identifiers

PMID31440234
PMCPMC6692769

What OpenQuestion holds

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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.