Publications by authors named "Gaia Piccioni"
Microglia, traditionally regarded as innate immune cells in the brain, drive neuroinflammation and synaptic dysfunctions in the early phases of Alzheimer disease (AD), acting upstream to Aβ accumulation. Colony stimulating factor 1-receptor (CSF-1R) is predominantly expressed on microglia and its levels are significantly increased in neurodegenerative diseases, possibly contributing to the chronic inflammatory microglial response. On the other hand, CSF-1R inhibitors confer neuroprotection in preclinical models of neurodegenerative diseases.
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- Many clinical trials on anti-amyloid agents for Alzheimer's disease have failed, calling the amyloid hypothesis into question.
- Researchers are now focusing on microglia, non-neuronal cells that are crucial for brain development and synaptic remodeling, as potential targets for new treatments.
- The review discusses how microglia contribute to synaptic loss and neuroinflammation in Alzheimer's, suggesting that targeting these cells could lead to effective disease-modifying therapies.
Article Synopsis
- Comprehensive omics and functional enrichment research in oncology has led to the development of treatments based on molecular pathways, with the potential for use in other medical fields like psychiatry and neurology.
- The review focuses on the β-site amyloid precursor protein cleaving enzyme (BACE) and its impact on neurological and psychiatric disorders, suggesting a shared genetic and biological basis among conditions like Alzheimer's and autism.
- The authors argue for a shift from traditional symptom-focused models to biology-based strategies in clinical neurology and psychiatry, proposing that advanced techniques in systems biology could enhance therapeutic approaches.
In this review, we focus on the emerging roles of microglia in the brain, with particular attention to synaptic plasticity in health and disease. We present evidence that ramified microglia, classically believed to be "resting" (i.e.
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