The role of microtubule proteins TUBB2A, TUBB3, and TUBB4B in neuronal dysfunction in Alzheimer’s disease: a bioinformatics analysis

JOURNAL/agad/04.03/02274129-202512000-00003/figure1/v/2025-10-02T155305Z/r/image-tiff Alzheimer’s disease represents a significant public health challenge, characterized by progressive cognitive decline and memory impairment. This study focuses on the roles of the microtubule proteins TUBB2A, TUBB3, and TUBB4B, which are critical components of β-tubulin and essential for guanosine triphosphate binding that promotes microtubule stability. Utilizing gene expression datasets from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO), we conducted differential expression analysis and correlation assessments. Our results reveal significant downregulation of TUBB2A, TUBB3, and TUBB4B in Alzheimer’s disease, which correlates with the severity of neurofibrillary tangles and Mini-Mental State Examination scores. This study shows that the downregulation of β-tubulin inhibits tubulin assembly. From a dynamic perspective, it investigates the specific mechanisms by which β-tubulin genes such as TUBB2A, TUBB3, and TUBB4B contribute to Alzheimer’s disease. The research further explores the key roles of these β-tubulin genes in maintaining microtubule dynamic instability and functional integrity, which provides new insights for elucidating the molecular mechanisms underlying Alzheimer’s disease.