Neurodegenerative diseases are a class of nervous system disorders characterized by delayed onset and selective neuronal dysfunction, which are closely associated with aging.Given the challenges associated with early detection and the irreversible nature of the condition, the pursuit of specific biomarkers has emerged as a critical component of disease prevention strategies.Optical coherence tomography angiography (OCTA) generates images which exhibit near-histological resolution without the requirement for contrast agent injection, demonstrating superior sensitivity compared to fundus photography. OCTA has the ability to identify and evaluate neurodegenerative diseases via the quantitative analysis of retinal parameters. The OCTA of the retina and choroid has been verified as a highly sensitive instrument for detecting microvascular abnormalities in both ocular and systemic retinal disorders. This review focuses on the application of OCTA in various neurodegenerative diseases, such as Alzheimer′s disease, Parkinson disease, Huntington′s disease, amyotrophic lateral sclerosis and Wolfram syndrome, with the aim of providing a reference for the early diagnosis and prevention of neurodegenerative diseases.

Neurodegenerative diseases are a class of nervous system disorders characterized by delayed onset and selective neuronal dysfunction, which are closely associated with aging.Given the challenges associated with early detection and the irreversible nature of the condition, the pursuit of specific biomarkers has emerged as a critical component of disease prevention strategies.Optical coherence tomography angiography (OCTA) generates images which exhibit near-histological resolution without the requirement for contrast agent injection, demonstrating superior sensitivity compared to fundus photography. OCTA has the ability to identify and evaluate neurodegenerative diseases via the quantitative analysis of retinal parameters. The OCTA of the retina and choroid has been verified as a highly sensitive instrument for detecting microvascular abnormalities in both ocular and systemic retinal disorders. This review focuses on the application of OCTA in various neurodegenerative diseases, such as Alzheimer′s disease, Parkinson disease, Huntington′s disease, amyotrophic lateral sclerosis and Wolfram syndrome, with the aim of providing a reference for the early diagnosis and prevention of neurodegenerative diseases.

Objective:To investigate the regulatory effects of mitofusin 1 (MFN1) on lipopolysaccharide (LPS)-induced Raw264.7 mouse macrophages pyroptosis and to provide reference for further study on the prevention of inflammation and fibrosis caused by macrophage dysfunction.Methods:Raw264.7 mouse macrophages were cultured in vitro and used to construct a model of LPS-induced pyroptosis. CCK-8 staining, PI staining, LDH release assay and Western blot were used to verify the Raw264.7 pyroptosis induced by LPS. MFN1 expression was detected by Western blot. DCFH-DA probe was used to detect the synthesis of total reactive oxygen species (ROS); Mito-SOX was used to detect mitochondrial ROS; JC-1 mitochondrial membrane potential was detected by fluorescence probe to reflect mitochondrial damage. Based on Ubibrowser database, it was predicted that MFN1 could bind to a variety of E3 ubiquitin ligases. Then, immunofluorescence and co-immunoprecipitation (CO-IP) were used to analyze MFN1 ubiquitination. An overexpression plasmid for MFN1 was constructed and transfected into Raw264.7 cells to detect the changes in pyroptosis and mitochondrial function. Results:LPS could induce the pyroptosis of Raw264.7 cells and mitochondrial dysfunction. MFN1 expression was decreased after LPS stimulation. Ubiquitinated MFN1 was detected by CO-IP. Ubiquitination inhibitor MG-132 inhibited LPS-induced expression of pyroptosis-related proteins including NLRP3, Pro-caspase-1, Caspase-1, IL-1β and IL-18 and improved mitochondrial function. MFN1 overexpression relieved the mitochondrial dysfunction and pyroptosis of Raw264.7 cells induced by LPS.Conclusions:The ubiquitination of MFN1 induced by LPS was involved in mitochondrial dysfunction and macrophage pyroptosis, suggesting that MFN1 was a potential target for the treatment of macrophage-induced inflammation and related diseases.