Polyphenols and microglial dynamics in neurodegenerative diseases: mechanistic advances and therapeutic perspectives

Targeting Neutrophil Extracellular Traps in Neuroinflammation: A Therapeutic Perspective on Neurodegenerative Diseases

The protective and deleterious roles of NETs are investigated and how this knowledge may reveal new therapeutic strategies to modulate neurodegenerative diseases and preserve neural integrity are investigated, offering valuable insights for potential applications in clinical practice.

Neuroinflammatory mechanisms and immunomodulatory therapies in Alzheimer's disease

This review synthesises current understanding of neuroinflammatory pathogenesis in AD, with emphasis on Microglial polarisation (M1/M2), Disease-Associated Microglia (DAM), TREM2 signalling, and reactive astrocyte conversion.

Neuron-Derived Neuroinflammation in Neurodegenerative Diseases: Mechanisms and Intervention Prospects.

Neurodegenerative diseases represent a major global public health challenge, imposing substantial societal and economic burdens. Their complex pathogenesis and limited therapeutic options underscore an urgent need for new paradigms. Emerging evidence indicates that dysregulation of the brain's immune microenvironment is a critical driver of disease progression. Conventional wisdom posits that peripheral immune cells and central glial cells serve as the primary initiators of neuroimmune responses, whereas neurons are regarded merely as passive recipients of inflammatory damage. Emerging evidence suggests that upon receiving pathological signals in the central nervous system, neurons may become more vulnerable and participate in the onset of neuroimmune processes, positioning them as potential targets for early intervention in neurodegenerative diseases. This article systematically reviews the contribution of neuron-derived immune-inflammatory responses in neurodegenerative diseases and potential intervention strategies. We first outline the capacity of neurons to regulate neuroimmune responses and detail the underlying molecular mechanisms. Then we compare the specific mechanisms by which neurons with different susceptibility drive and amplify neuroinflammation in various neurodegenerative diseases such as alzheimer's disease, parkinson's disease, amyotrophic lateral sclerosis, vascular cognitive impairment, and transformed these mechanisms into intervention strategies targeting neurons,. This article aims to break through the traditional concept of passive neuronal damage, systematically integrate intervention strategies that shift from targeting peripheral immune and glial cells to regulating neuron-derived immunity, thereby providing a new theoretical framework for overcoming current clinical limitations and identifying effective therapeutic targets for the prevention and treatment of neurodegenerative diseases.

Nanomedicine targeting neuroinflammatory pathways in Alzheimer’s disease: a new frontier in inflammopharmacology

Targeting Microglial Receptors for Alzheimer’s Disease: Translational Barriers from Bench to Bedside

Alzheimer’s disease (AD) remains a major neurodegenerative challenge with limited therapeutic options. Microglia, the resident immune cells of the central nervous system, shape key pathological processes in AD, including amyloid-beta (Aβ) clearance, neuroinflammation, tau pathology, and synaptic homeostasis. Accordingly, microglial receptors that regulate microglial sensing, phagocytosis, and inflammatory signaling have emerged as candidates for disease-modifying interventions. However, translation from preclinical discovery to clinical benefit is impeded by multiple barriers, including stage-dependent receptor functions, peripheral off-target effects, compensatory signaling within interconnected receptor networks, biomarker deficiencies, and species differences, all of which are key bottlenecks detailed in this review. We summarize preclinical and clinical progress in therapeutics targeting microglial receptors; analyze these critical translational bottlenecks; and discuss potential strategies including precision delivery, humanized experimental systems, and biomarker-forward trial designs, with the goal of supporting rigorously designed and biomarker-informed clinical translation.

Targeting Neurodegeneration With Naringenin: Mechanistic Perspectives and Therapeutic Implications

NAR has demonstrated the ability to reduce amyloid-β plaque deposition, inhibit α-synuclein aggregation, preserve dopaminergic neurons, modulate immune responses in multiple sclerosis, and improve functional recovery after spinal cord injury.