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Neuroinflammatory Diseases / Alzheimer Disease / Alzheimer's Disease · Journal article
Cellular Signalling · June 26, 2026
A consensus or society position rather than new primary data.
This is a narrative review of AD pathophysiology and therapeutic strategy, positioning neuroinflammation as a central driver of disease progression and identifying microglial activation, TREM2 signaling, NLRP3 inflammasome, and complement dysregulation as clinically actionable targets. The review advocates for biomarker-guided patient selection, stage-specific intervention during prodromal and early symptomatic phases, and multi-target therapeutic approaches combining amyloid, tau, and neuroinflammatory modulation, but does not present new experimental or clinical trial data.
Journal article. Alzheimer's disease patients across disease stages (prodromal to symptomatic); general population for early detection and risk stratification..
Neuroinflammation positioned as central driver, not merely secondary response to amyloid and tau pathology. Microglial activation pathways (TREM2 signaling, NLRP3 inflammasome, complement dysregulation) identified as most clinically actionable targets. Modulation of innate immune pathways most likely to confer benefit during prodromal and early symptomatic stages when neuroinflammatory responses remain partially adaptive.
Long-term clinical impact and safety profiles of aducanumab and lecanemab stated as 'under evaluation' without specific trial results. Recent FDA approvals of aducanumab and lecanemab represent disease-modifying advances, though long-term efficacy and safety profiles remain under evaluation.
Clinicians should consider stage-specific neuroinflammatory modulation strategies during early disease and employ biomarker-guided patient selection for anti-amyloid therapies. Multi-target approaches and inflammatory biomarker monitoring are emerging as precision medicine strategies, though evidence for individual immune targets remains under investigation.
A narrative review synthesizing current understanding of AD pathogenesis and therapeutic strategies; positions neuroinflammation as central and identifies actionable immune targets, but provides no new empirical data or comparative efficacy evidence.
As stated by the source record.
Clinicians should consider stage-specific neuroinflammatory modulation strategies during early disease and employ biomarker-guided patient selection for anti-amyloid therapies. Multi-target approaches and inflammatory biomarker monitoring are emerging as precision medicine strategies, though evidence for individual immune targets remains under investigation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Alzheimer's disease (AD) is a multifactorial and progressive neurodegenerative disorder characterized by complex interactions among amyloid-β (Aβ) deposition, tau protein hyperphosphorylation, neuroinflammation, oxidative stress, metal dyshomeostasis, and impaired autophagy. Increasing evidence positions neuroinflammation not merely as a secondary response but as a central driver of disease progression, dynamically interacting with amyloid and tau protein pathology and contributing to synaptic dysfunction and neuronal loss. Among inflammatory mechanisms, microglial activation pathways-particularly TREM2 signaling, NLRP3 inflammasome activation, and complement cascade dysregulation-are currently the most clinically actionable targets, supported by genetic, biomarker, and therapeutic evidence. Emerging data suggest that modulation of innate immune pathways is most likely to confer benefit during the prodromal and early symptomatic stages of AD, when neuroinflammatory responses remain partially adaptive and neuronal networks retain functional reserve. Despite decades of drug development, many candidates have failed due to limited efficacy or safety concerns. Recent FDA approvals of anti-amyloid monoclonal antibodies, including aducanumab and lecanemab, represent important advances toward disease-modifying therapy, although their long-term clinical impact and safety profiles remain under evaluation. These developments underscore the importance of biomarker-guided patient selection, disease-stage stratification, and vigilant safety monitoring, particularly regarding amyloid-related imaging abnormalities. Therapeutic strategies are increasingly shifting toward multi-target approaches that integrate amyloid modulation, tau protein-directed interventions, and attenuation of maladaptive neuroinflammatory responses. Concurrently, inflammatory mediators and peripheral metabolic biomarkers are gaining recognition as tools for early detection, risk stratification, and therapeutic response monitoring, potentially enabling precision-based intervention. This review synthesizes current understanding of AD pathogenesis through an inflammation-centered framework, highlighting clinically actionable immune pathways and stage-specific therapeutic windows. By integrating mechanistic insights with biomarker-driven strategies, we aim to delineate translational paths toward more precise, safe, and clinically meaningful disease modification.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.