As the global population ages, neurodegenerative diseases, particularly Alzheimer's disease (AD), have become a major public health concern. AD is the most prevalent neurodegenerative disorder, accounting for 60-80% of cases, and is characterized by progressive cognitive and memory decline due to neuronal loss. Current pharmacological treatments primarily offer symptomatic relief rather than a cure. Recent research has highlighted the role of vitamin D in neuroprotection, owing to its antioxidant, anti-inflammatory, and neuroprotective properties, as well as its ability to maintain blood-brain barrier integrity and regulate amyloid-beta (Aβ) clearance. Another emerging noninvasive therapeutic approach is Low-Level Laser Therapy (LLLT), a form of photobiomodulation (PBM) that has been shown to enhance neuronal function, reduce oxidative stress, inflammation, and Aβ deposition, and potentially increase vitamin D levels. This review examines the interplay between LLLT, vitamin D, and oxidative stress in AD pathophysiology. Findings suggest that LLLT can stimulate mitochondrial function, enhance synaptic plasticity, and improve cognitive performance in preclinical and clinical studies. Furthermore, LLLT has been reported to modulate immune responses, promote neurogenesis, and facilitate vitamin D synthesis by activating cytochrome c oxidase (CCO), which plays a crucial role in mitochondrial energy production. However, while promising, further in vivo and clinical trials are required to optimize treatment protocols and establish standardized guidelines for LLLT application, particularly in enhancing vitamin D levels, in AD patients. CLINICAL TRIAL NUMBER: Not applicable.