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A Path Toward Precision Medicine for Neuroinflammatory Mechanisms in Alzheimer's Disease
Open accessAbstract
Neuroinflammation commences decades before Alzheimer’s disease (AD) clinical onset and represents one of the earliest pathomechanistic alterations throughout AD its continuum. Large-scale genome-wide association studies point out several genetic variants - TREM2, CD33, PILRA, CR1, MS4A, CLU, ABCA7, EPHA1, and HLA-DRB5-HLA-DRB1 - potentially linked to neuroinflammation. Most of these genes are involved in proinflammatory intracellular signaling, cytokines/interleukins cell turn-over, synaptic activity, lipid metabolism, and vesicle trafficking. Proteomic studies indicate that a plethora of interconnected aberrant molecular pathways, set off and perpetuated by TNF-α, TGF-β, IL-1β, and the receptor protein TREM2, are involved in neuroinflammation. Microglia and astrocytes are key cellular drivers and regulators of neuroinflammation. Under physiological conditions, they are important for neurotransmission and synaptic homeostasis. In AD, there is a turning point throughout its pathophysiological evolution where glial cells sustain an overexpressed inflammatory response that synergizes with amyloid-β and tau accumulation, and drives synaptotoxicity and neurodegeneration in a self-reinforcing manner. Despite a strong therapeutic rationale, previous clinical trials investigating compounds with anti-inflammatory properties, including non-steroidal anti-inflammatory drugs (NSAIDs) did not achieve primary efficacy endpoints. It is conceivable that study design issues, including the lack of diagnostic accuracy and biomarkers for target population identification and proof-of-mechanism may partially explain the negative outcomes. However, a recent meta-analysis indicates a potential biological effect of NSAIDs. In this regard, candidate fluid biomarkers of neuroinflammation are under analytical/clinical validation, i.e. TREM2, IL-1β, MCP-1, IL-6, TNF-α receptor complexes, TGF-β, YKL-40. PET radio-ligands are investigated to accomplish in-vivo and longitudinal regional exploration of neuroinflammation. Biomarkers tracking different molecular pathways (body fluid matrixes) along with brain neuroinflammatory endophenotypes (neuroimaging markers), can untangle temporal-spatial dynamics between neuroinflammation and other AD pathophysiological mechanisms. Robust biomarker-drug co-development pipelines are expected to enrich large-scale clinical trials testing new-generation compounds active, directly or indirectly, on neuroinflammatory targets and displaying putative disease-modifying effects: novel NSAIDs, AL002 (anti-TREM2 antibody), anti-Aβ protofibrils (BAN2401), and AL003 (anti-CD33 antibody). As a next step, taking advantage of breakthrough and multimodal techniques coupled with a systems biology approach is the path to pursue for developing individualized therapeutic strategies targeting neuroinflammation under the framework of precision medicine.
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“mitochondrial dysfunction—with reactive oxygen species (ROS) accumulation and neuroinflammation driving microglial activation—plays a central role in AD pathogenesis [56]”
From Theranostic Nanoplatforms for Alzheimer's Disease: A Critical Analysis of Conceptual Contradictions (2026) · cites this paper as [56]
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- Presented at the 11thClinical Trials on Alzheimer's Disease (CTAD) Conference October 24–272018
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“Such neuroinflammation promotes the early progression of AD, with it being among the earliest pathologic changes observed in the disease (Hampel and others 2020).”
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“Similarly, the suppression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and microglial activation suggests that ReA dampens the chronic neuroinflammatory response, a key driver of disease progression 37,38 .”
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“…disease, such as monoclonal antibodies (Salloway et al., 2022; van Dyck et al., 2023), there is growing concern about amyloid-related imaging abnormalities with hemosiderin deposition (ARIA-H), a key safety issue in clinical trials and treatment (Hampel et al., 2020; Sperling et al., 2011).”
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Diagnose It Yourself: Will There Be a Home Test Kit for Alzheimer’s disease?
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The circRNA and Role in Alzheimer’s Disease: From Regulation to Therapeutic and Diagnostic Targets
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“For instance, TNF-α can stimulate γ-secretase activity, which results in increased levels of Aβ and the following cognitive decline in AD [84].”
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“7 The microglial cells ’ activation causes the production of cytokines, which, in turn, causes chronic inflammation in the neurological system.”
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“Such complexity renders AD a major challenge in contemporary neuroscience and translational research (Hampel et al. 2020).”
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Systemic inflammation causes microglial dysfunction with a mixed AD-like pathologyPreprint
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Systemic Inflammation Causes Microglial Dysfunction with a Mixed AD-Like Pathology.Preprint
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Metadata
- Authors
- Hampel, H., Caraci, F., Cuello, A. C., Caruso, G., Nisticò, R., Corbo, M., Baldacci, F., Toschi, N., Garaci, F., Chiesa, P. A., Verdooner, S. R., Akman-Anderson, L., Hernández, F., Ávila, J., Emanuele, E., Valenzuela, P. L., Lucía, A., Watling, M., Imbimbo, B. P., Vergallo, A., & Lista, S.
- Affiliations
- Sorbonne Université (FR)
- University of Catania (IT)
- University of Oxford (GB)
- I.R.C.C.S. Oasi Maria SS (IT)
- University of Rome Tor Vergata (IT)
- University of Pisa (IT)
- Centre National de la Recherche Scientifique (FR)
- Consejo Superior de Investigaciones Científicas (ES)
- Universidad de Alcalá (ES)
- Research Institute Hospital 12 de Octubre (ES)
- Chiesi (Italy) (IT)
- Corresponding author
- Hampel, Harald
- ORCID
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2020-03-31
- Volume
- 11
- Pages
- 456-456
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC7137904
- OpenAlex
- W3014540555
- Cited by
- 360
- References
- 297
- Citations by year
- 2026: 43 · 2025: 53 · 2024: 53 · 2023: 66 · 2022: 69 · 2021: 49 · 2020: 22
- FWCI
- 5.13
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, cc-by)
- Biblos-e Archivo (Universidad Autónoma de Madrid) (submittedVersion, cc-by)
- ABACUS. Repositorio de Producción Científica (Universidad Europea) (submittedVersion, cc-by-nc-nd)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion, other-oa)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Hispana (submittedVersion)
- Funders
- AXA Research Fund
- Eisai
- Sorbonne Université
- Fondation pour la Recherche sur Alzheimer
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, neuroinflammation, TREM2, microglia, astrocytes, amyloid-beta, tau protein, synaptotoxicity, neurodegeneration, genetic risk variants, cytokines, TNF-α, IL-1β, TGF-beta, biomarkers, positron emission tomography, nonsteroidal anti-inflammatory drugs, disease-modifying therapy, precision medicine
- MeSH terms
- Cell Self Renewal, Alzheimer Disease, Animals, Humans, Signal Transduction, Cytokines, Neurogenic Inflammation, Proteomics, Systems Biology, Lipid Metabolism, Genome-Wide Association Study, Precision Medicine
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