ReviewJournal of neuroinflammation2026
Convergence of neuroinflammation across major neurotropic viral exposomes in AD and ADRD.
Review in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundAlzheimer's disease (AD) and Alzheimer's disease-related dementias (ADRD) are multifactorial neurodegenerative disorders driven by complex interactions among genetic susceptibility, aging, and environmental exposures. Growing epidemiological and mechanistic evidence implicates neurotropic viral exposomes, defined as cumulative lifetime viral infections, as significant contributors to AD risk. Viral encephalitis and common viral infections, including herpes simplex virus type 1 (HSV-1), human immunodeficiency virus (HIV), cytomegalovirus (CMV), SARS-CoV-2, and influenza, have been associated with an increased incidence of AD/ADRD; however, the molecular mechanisms underlying these associations remain incompletely understood.
methodsA systematic literature review was conducted using PubMed, Web of Science, Scopus, and Google Scholar (1990-2025) to identify epidemiological, experimental, and mechanistic studies linking viral infections to AD-related pathology. Systems biology approaches were applied using Cytoscape, STRING, KEGG, WikiPathways, and Ingenuity Pathway Analysis to construct protein-protein interaction networks and identify convergent biological processes shared between AD and viral host-response pathways. Functional enrichment analyses focused on neuroinflammation, amyloid-β (Aβ) metabolism, tau pathology, autophagy, and blood-brain barrier (BBB) integrity.
resultsAcross diverse viral infections, strong convergence was observed in innate immune activation pathways, including microglial priming and NLRP3 inflammasome signaling, accompanied by chronic production of proinflammatory cytokines (IL-1β, TNF-α, IFN-γ). Multiple viruses modulated amyloidogenic APP processing, impaired Aβ clearance, promoted tau hyperphosphorylation, disrupted autophagy-lysosomal systems, and compromised BBB integrity. Systems-level analyses revealed overlapping signaling hubs, including NF-κB, MAPK, PI3K-Akt, and cGAS-STING that amplify neurodegenerative cascades, with effects most pronounced in genetically susceptible populations such as APOE4 carriers.
conclusionsCollectively, current evidence supports a mechanistic link between viral exposomes and AD/ADRD mediated through convergent neuroinflammatory, and proteostatic pathways. Although viral infections alone are unlikely to be sufficient to cause AD, recurrent or persistent viral exposures may act as potent disease modifiers that accelerate neurodegenerative processes. Integrating viral biomarkers, genetic risk stratification, and systems biology approaches offers promising opportunities for early diagnosis, prevention, and development of mechanism-guided therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.