Evidence map›Paper›PMID 25698933›Full record

ReviewFrontiers in cellular neuroscience2015

Systemic inflammation and the brain: novel roles of genetic, molecular, and environmental cues as drivers of neurodegeneration.

Roman Sankowski, Simone Mader, Sergio Iván Valdés-Ferrer

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 4 pooled it
14.1field-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

198 citing papers in PubMed, 4 syntheses or guidelines pooled it, 345 citations in OpenAlex.

  1. Pooled it
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  5. Trial
  6. Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  10. Metabolic syndrome is associated with accelerated brain aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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138 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 3 institutions in 2 countries.

Roman SankowskiElmezzi Graduate School of Molecular Medicine , Manhasset, NY , USA ; Feinstein Institute for Medical Research , Manhasset, NY , USA.
Simone MaderFeinstein Institute for Medical Research , Manhasset, NY , USA.
Sergio Iván Valdés-FerrerElmezzi Graduate School of Molecular Medicine , Manhasset, NY , USA ; Feinstein Institute for Medical Research , Manhasset, NY , USA ; Department of Neurology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán , México City , Mexico.
Feinstein Institute for Medical Research · USIcahn School of Medicine at Mount Sinai · USInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nervous and immune systems have evolved in parallel from the early bilaterians, in which innate immunity and a central nervous system (CNS) coexisted for the first time, to jawed vertebrates and the appearance of adaptive immunity. The CNS feeds from, and integrates efferent signals in response to, somatic and autonomic sensory information. The CNS receives input also from the periphery about inflammation and infection. Cytokines, chemokines, and damage-associated soluble mediators of systemic inflammation can also gain access to the CNS via blood flow. In response to systemic inflammation, those soluble mediators can access directly through the circumventricular organs, as well as open the blood-brain barrier. The resulting translocation of inflammatory mediators can interfere with neuronal and glial well-being, leading to a break of balance in brain homeostasis. This in turn results in cognitive and behavioral manifestations commonly present during acute infections - including anorexia, malaise, depression, and decreased physical activity - collectively known as the sickness behavior (SB). While SB manifestations are transient and self-limited, under states of persistent systemic inflammatory response the cognitive and behavioral changes can become permanent. For example, cognitive decline is almost universal in sepsis survivors, and a common finding in patients with systemic lupus erythematosus. Here, we review recent genetic evidence suggesting an association between neurodegenerative disorders and persistent immune activation; clinical and experimental evidence indicating previously unidentified immune-mediated pathways of neurodegeneration; and novel immunomodulatory targets and their potential relevance for neurodegenerative disorders.

Indexed as

anti-brain antibodiesautoimmune disordersconnectomeHMGB1neurodegenerationsystemic inflammation and sepsisTNF

Identifiers

PMID25698933
PMCPMC4313590
OpenAlexW2158978919

What OpenQuestion 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 OpenQuestion graph.