ReviewMolecular psychiatry2026
Hospital-treated infection associated with Alzheimer's disease pathology: underlying mechanisms.
Review in Molecular psychiatry, 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
importanceGrowing epidemiological and mechanistic evidence indicates that infections substantially increase the risk of Alzheimer's disease (AD) and related dementias. Systemic immune activation and pathogen persistence may act as upstream triggers accelerating neurodegenerative cascades.
objectiveTo synthesize recent evidence on infection-driven mechanisms contributing to AD pathology, emphasizing how systemic and central immune activation influence amyloid-beta (Aβ) aggregation, tau pathology, blood-brain barrier (BBB) dysfunction, and neuroinflammation. DESIGN, SETTING, AND
participantsThis expert review integrates data from large epidemiological cohorts, neuropathological analyses, and mechanistic studies in both human and animal models to address innate and adaptive immune mechanisms linking infection to AD pathogenesis. EXPOSURES: Systemic and central nervous system (CNS) infections, including sepsis, pneumonia, viral, and chronic bacterial infections, as well as hospital-treated infections, that trigger inflammatory and immune signaling cascades impacting the brain's structural and molecular integrity.
resultsInfections activate the innate immune system through toll-like receptors and inflammasomes (NOD-like receptor family pyrin domain-containing 3 (NLRP3), linear ubiquitin assembly complex (LUBAC)), driving chronic neuroinflammation, pyroptosis, and the release of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) speck that cross-seeds Aβ and tau aggregation. Additionally, cytokine-induced upregulation of interferon-induced transmembrane protein 3 (IFITM3) enhances γ-secretase activity, thereby increasing Aβ production. Therefore, peripheral inflammation compromises BBB integrity, while extracellular vesicles propagate inflammatory cargoes across the neurovascular unit. Consequently, the expansion of cytotoxic CD8⁺ T cells and the alteration of Th1/Th17 profiles are linked to adaptive immunity and neurodegeneration. Moreover, epidemiologic data show reduced AD risk following herpes zoster, Tdap/Td (tetanus, diphtheria, and acellular pertussis (Tdap) and tetanus and diphtheria (Td) vaccines), and pneumococcal vaccination, supporting immune modulation as a preventive strategy. CONCLUSIONS AND RELEVANCE: Infection-driven immune activation represents a key modifiable pathway in AD pathogenesis, highlighting novel diagnostic and therapeutic targets focused on the inflammasome.
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.