Interactions among Interleukin‐1β, Amyloid‐β, and Tau drive synaptic deficits in a mouse model of sporadic Alzheimer's disease induced by HSV‐1 infection
Our findings suggest that IL-1β-mediated neuroinflammation plays a pivotal role in driving synaptic dysfunction during the early stages of this mouse model of AD. The lower IL-1β levels and reduced synaptic deficits observed in mice lacking either Aβ or pTau indicate that these key AD hallmarks contribute to IL-1β accumulation, thereby triggering a vicious circle in the pathophysiology of synaptic dysfunction in AD.
Authors
- Roberto Piacentini (ORCID: https://orcid.org/0000-0003-4215-1643)
- Giovanna De Chiara (ORCID: https://orcid.org/0000-0002-2219-6097)
- Domenica Donatella Li Puma (ORCID: https://orcid.org/0000-0001-6729-6967)
- Gulia Puliatti
- Claudio Grassi
- Giammarco Boni
- Anna Teresa Palamara
- Marco Rinaudo
Institutions
- Università Cattolica del Sacro Cuore (IT)
- Istituto Superiore di Sanità (IT)
- Agostino Gemelli University Polyclinic (IT)
- Istituto di Farmacologia Traslazionale (IT)
- Istituti di Ricovero e Cura a Carattere Scientifico (IT)
- Sapienza University of Rome (IT)
Publication Details
- Journal
- Alzheimer s & Dementia
- Published
- 2025-12-01
- DOI
- https://doi.org/10.1002/alz70855_102964
- Primary Topic
- Alzheimer's disease research and treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00