Abstract: Sulforaphane (SFN) is a naturally occurring compound that has been demonstrated to possess a range of biological activities, including antioxidant, anti-inflammatory, detoxifying, anti-glycation, and immunomodulatory effects. Nuclear factor erythroid-2-related factor 2 (Nrf2) has been identified as a key target for the action of sulforaphane (SFN). This review summarises recent advances in research concerning the functional mechanisms and roles of SFN-activated Nrf2 signalling pathways in various neurological disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, epilepsy, stroke, and traumatic brain injury. The process of interaction between NRF2-Keap1 (Kelch-like ECH-associated protein 1) has been extensively documented. The initial step in this process involves the binding of Nrf2 to Keap1, which subsequently leads to the ubiquitination and subsequent degradation of Nrf2. Upon stimulation by activators such as SFN or reactive oxygen species (ROS), Nrf2 dissociates from Keap1, translocates to the nucleus, and binds to Maf proteins. This process initiates the transcription of downstream genes regulated by the antioxidant response element (ARE), including heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and glutamate-cysteine ligase catalytic subunit (GCLC). Consequently, this enhances the cellular antioxidant capacity. This article aims to systematically review dietary sources of sulforaphane (SFN) and its potential role, through the activation of the Nrf2 signaling pathway, in intervening in and delaying the progression of various neurological diseases, thereby providing a scientific basis for developing SFN-based dietary strategies for neurological health.