c-Jun, a core component of the activating protein-1 (AP-1) transcription factor complex, regulates cellular processes including proliferation, differentiation, survival, apoptosis, and oncogenesis. c-Jun functions by dimerizing to bind DNA and modulates the expression of genes such as Bcl-2, cyclin D1, and pro-inflammatory cytokines, enabling context-dependent transcriptional control. Its role in neurodegenerative diseases has gained attention due to its regulation of oxidative stress, inflammation, and apoptosis. In Parkinson's disease, Alzheimer's disease, and Huntington's disease, dysregulated c-Jun expression accelerates dopaminergic neuron loss via oxidative damage, contributes to amyloid-β-induced synaptic toxicity, and mediates neuronal apoptosis and inflammation, respectively. Despite its degenerative role, c-Jun also promotes axonal regeneration and stress adaptation, revealing a dual function that depends on context and stimulus severity. This paradox underscores its ability to promote survival under mild stress and apoptosis under chronic damage. Emerging therapeutic strategies targeting c-Jun-via small-molecule inhibitors (e.g., SP600125), RNA interference, or modulation of upstream c-Jun N-terminal kinase (JNK)-are being explored. However, challenges remain in achieving specificity, as c-Jun's ubiquitous expression raises concerns about off-target effects. This review highlights recent advances in understanding c-Jun's complex role in neurodegeneration and its therapeutic potential, emphasizing its value as both a mechanistic regulator and a target for preserving neuronal integrity in neurodegenerative diseases.