Evidence map›Paper›PMID 40650013›Full record

ReviewInternational journal of molecular sciences2025

The Inflammatory Nexus: Unraveling Shared Pathways and Promising Treatments in Alzheimer's Disease and Schizophrenia.

Aurelio Pio Russo, Ylenia Pastorello, Lóránd Dénes, Klara Brînzaniuc, Jerzy Krupinski, Mark Slevin

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Aurelio Pio RussoDepartment of Anatomy and Embryology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mureş, 540139 Târgu Mureş, Romania.ORCID 0009-0003-7672-2798
Ylenia PastorelloDepartment of Anatomy and Embryology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mureş, 540139 Târgu Mureş, Romania.ORCID 0009-0004-3833-0184
Lóránd DénesDepartment of Anatomy and Embryology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mureş, 540139 Târgu Mureş, Romania.ORCID 0009-0008-8319-8134
Klara BrînzaniucDepartment of Anatomy and Embryology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mureş, 540139 Târgu Mureş, Romania.
Jerzy KrupinskiDepartment of Neurology, MútuaTerrassa University Hospital, 08221 Barcelona, Spain.
Mark SlevinCentre for Advanced Medical and Pharmaceutical Research, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mureş, 540139 Târgu Mureş, Romania.ORCID 0000-0003-3767-4861

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) and schizophrenia are traditionally considered distinct clinical entities, yet growing evidence highlights substantial overlap in their molecular and neuroinflammatory pathogenesis. This review explores current insights into the shared and divergent mechanisms underlying these disorders, with emphasis on neuroinflammation, autophagy dysfunction, blood-brain barrier (BBB) disruption, and cognitive impairment. We examine key signaling pathways, particularly spleen tyrosine kinase (SYK), the mechanistic (or mammalian) target of rapamycin (mTOR), and the S100 calcium-binding protein B (S100B)/receptor for advanced glycation end-products (RAGE) axis, that link glial activation, excitatory/inhibitory neurotransmitter imbalances, and impaired proteostasis across both disorders. Specific biomarkers such as S100B, matrix metalloproteinase 9 (MMP9), and soluble RAGE show promise for stratifying disease subtypes and predicting treatment response. Moreover, psychiatric symptoms frequently precede cognitive decline in both AD and schizophrenia, suggesting that mood and behavioral disturbances may serve as early diagnostic indicators. The roles of autophagic failure, cellular senescence, and impaired glymphatic clearance are also explored as contributors to chronic inflammation and neurodegeneration. Current treatments, including cholinesterase inhibitors and antipsychotics, primarily offer symptomatic relief, while emerging therapeutic approaches target upstream molecular drivers, such as mTOR inhibition and RAGE antagonism. Finally, we discuss the future potential of personalized medicine guided by genetic, neuroimaging, and biomarker profiles to optimize diagnosis and treatment strategies in both AD and schizophrenia. A greater understanding of the pathophysiological convergence between these disorders may pave the way for cross-diagnostic interventions and improved clinical outcomes.

Indexed as

Alzheimer DiseaseInflammationSchizophreniaAnimalsAntipsychotic AgentsAutophagyBiomarkersBlood-Brain BarrierHumansReceptor for Advanced Glycation End ProductsSignal TransductionAntipsychotic AgentsBiomarkersReceptor for Advanced Glycation End ProductsAlzheimer’s diseaseneuroinflammationreceptor for advanced glycation end-products (RAGE)S100 calcium binding protein B (S100B)schizophrenia

Identifiers

PMID40650013
PMCPMC12250212

What OpenQuestion holds

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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.