RNA splicing is an essential cellular process in which a series of protein-nucleic acid complexes cut and splice the products of gene transcription to generate mature RNA， and it plays an important role in maintaining the normal life activities of cells. Extensive studies have shown that proteins and nucleic acids associated with RNA splicing undergo the pathological changes such as aggregation in neurodegenerative diseases， and inadequate RNA splicing is observed in lesions. Genetic alterations within RNA splicing-related genes can cause neurodegenerative diseases. All these findings suggest that abnormalities in RNA splicing pathways may play a significant role in the pathogenesis of neurodegenerative diseases. This article reviews the research advances in the alterations of RNA splicing in common neurodegenerative diseases in terms of histopathology， biochemistry， and genetics， as well as related cell biology and animal models， in order to clarify their role in the pathogenesis of neurodegenerative diseases.
Alzheimer Disease ; Parkinson Disease

Objective To retrospectively analyze the results of serum beta-amyloid 42(Aβ42)tests conducted in the laboratory and explore potential issues associated with this testing.Methods All the Aβ42 test data collected up to the initiation of this study were compiled,and the positive rates for various diagnoses,including Alzheimer's disease(AD),cognitive decline,and dementia were ana-lyzed.Accuracy of the test kit was preliminarily validated using the kit's own reference,mouse brain tissue,and in vitro cultured cell-based reference samples.Results Data from 546 patients were col-lected,with 166 positive cases(positive rate of 30.4％).Among them,3 out of 6 AD patients tested positive;among 149 patients diagnosed with cognitive decline and 59 dementia patients,there were 29 and 24 positive cases respectively,with positive rates of 19.5％and 40.7％.The kit's detection of its own reference was affected by the serum matrix and failed to effectively detect positive mouse brain tissue and cellular reference samples.The kit's detection was generally unaffected by the amyloid precursor protein(APP)of Aβ,but it did not demonstrate good recovery rates for its own reference samples added to various clinical serum specimens.Conclusion The positive rate of serum Aβ42 test results in laboratory is lower than expected,and the accuracy of the test kit may require further improvement.