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"Lycium barbarum polysaccharides are considered the primary active ingredient of Lycium barbarum, and their therapeutic effects on retinal diseases have been extensively described. However, a systematic review and meta-analysis of these studies have not been conducted previously. This review aims to systematically review and meta-analyze published animal studies to investigate the mechanisms of the antioxidative, anti-inflammatory, anti-apoptotic, and neuroprotective effects of Lycium barbarum polysaccharides in rodent models of retinal diseases. To objectively and quantitatively compare the efficacy of Lycium barbarum polysaccharides in rodent models of retinal disease, a systematic review was conducted to search the PubMed and Web of Science databases (from inception to July 2024) for studies conducted in animals that met all a priori inclusion criteria. The included 27 studies reported outcomes on retinal structure (outer nuclear layer thickness) or function (electroretinogram b-wave amplitude). The methodological quality, assessed using the SYRCLE bias risk assessment tool, indicated that the overall risk of bias in the included literature was predominantly moderate. The results of the meta-analysis conducted using RevMan 5.4.1 software found that Lycium barbarum polysaccharides are protective against retinal injury in animal models, as evidenced by increases in the thickness of the outer nuclear layer and b-wave amplitude. The mechanisms involved include antioxidant effects, anti-inflammation, anti-apoptosis, and modulation of glia-driven neuroinflammation. Findings from this review confirm the protective actions of Lycium barbarum polysaccharides on retinal outer nuclear layer thickness and neuronal cells in rodent models of retinal diseases and may help propose strategies for future translational research on Lycium barbarum polysaccharides."

"Major depressive disorder is a complex psychiatric condition characterized by mood dysregulation, cognitive impairment, and somatic symptoms. Recent studies underscore the pivotal roles of neural regeneration and inflammation in its pathophysiology. This narrative review synthesizes emerging evidence linking neuroinflammatory pathways and impaired neurogenesis in major depressive disorder. We explore mechanisms including microglial activation, kynurenine pathway dysregulation, synaptic remodeling, and gut–brain axis alterations. Special emphasis is placed on recent discoveries highlighting molecular cross-talk between immune responses and neural plasticity. By mapping these interactions, we aim to advance understanding of major depressive disorder subtypes and support the development of inflammation-targeted therapies."

"The permanent functional deficits resulting from the inability of adult mammalian central nervous system neurons to regenerate after injury present a significant clinical challenge. While traditional stem cell transplantation strategies continue to encounter ethical concerns and the risk of immune rejection, this impasse has shifted regenerative medicine research toward targeting endogenous astrocytes. Due to their intrinsic plasticity, widespread distribution throughout the central nervous system, and affinity for neurodevelopmental lineage, astrocytes are a unique target for in situ neuronal regeneration. This review systematically elucidates the core regulatory network governing astrocyte transdifferentiation, identifying 10 key signaling pathways, such as Wnt signaling pathway, that form a cascade regulatory system. Directed overexpression of transcription factors such as NeuroD1, Ascl1, or Neurog2 can directly initiate neuronal phenotypic conversion. Meanwhile, small molecule compounds such as valproic acid combined with CHIR99021 activate endogenous neurogenic programs by inhibiting the bone morphogenetic protein signaling axis. Notably, polypyrimidine tract binding protein 1 (PTB) gene silencing significantly enhances transdifferentiation efficiency by suppressing the microRNA 124/re1 silencing transcription factor (miR-124/REST) feedback loop. From a translational perspective, a multidimensional evaluation system based on morphological, molecular marker, and electrophysiological properties has demonstrated considerable therapeutic potential. In stroke models, NeuroD1-mediated transdifferentiation replenished approximately 30% of lost cortical neurons and improved motor coordination, evidenced by enhanced performance in food pellet retrieval, grid walking, and cylinder tests compared with controls. In spinal cord injury studies, SOX2-induced glutamatergic neurons moderately reduced glial scar density by about 25%, permitting regenerating axons to pass through while preserving the supportive structure of scar. In neurodegenerative contexts, PTB inhibition yielded functionally mature dopaminergic neurons and reconstructed nigrostriatal pathways in Parkinson’s disease models. In Alzheimer’s disease models, adeno-associated virus-delivered NeuroD1 induced whole-brain neural circuit remodeling, generating 500,000 new neurons widely distributed across the cortex and hippocampus, accompanied by improved cognitive performance. Current technical limitations include off-target effects of adeno-associated virus vectors, which cause nonspecific gene expression and require rigorous validation via Cre-loxP lineage tracing. Transdifferentiation efficiency is also highly influenced by regional microenvironments: gray matter astrocytes show higher conversion rates than those in white matter, and oxidative stress increases apoptosis among newly generated neurons. Clinical translation is further constrained by the safety of delivery systems and the aging tissue microenvironment, where transforming growth factor beta 1 is often elevated. Ferroptosis inhibitors have been shown to nearly double the survival rate of transdifferentiated cells, offering a novel strategy to mitigate oxidative damage. Based on current evidence, astrocyte transdifferentiation enables neural functional recovery across multiple disease models through endogenous repair mechanisms. Future advances should focus on optogenetically inducible vectors for spatiotemporal precision, non-viral delivery systems to mitigate vector-related risks, and integration of long-term safety validation in non-human primates with single-cell multi-omics technologies to facilitate the clinical translation of personalized regenerative therapies."

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