Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline. This review examines the potential neuroprotective roles of neurosteroids like allopregnanolone (AlloP) and 24(S)-hydroxycholesterol (24(S)-HC) in AD. Multiple preclinical studies in rodent models demonstrate the ability of AlloP to promote neurogenesis, myelination, and anti-inflammatory effects via GABA receptor modulation. Enhanced AlloP levels reduced amyloid-beta pathology in an AD mouse model. The enzyme CYP46A1 converts cholesterol to 24(S)-HC which can exit the brain. CYP46A1 upregulation appears neuroprotective in some AD models through improved cholesterol homeostasis. Analysis of human AD patient brain tissues reveals reduced AlloP levels correlating with disease progression. Overall, these neurosteroids show promise as novel AD therapeutics by targeting pathogenic mechanisms like neurodegeneration, neuro inflammation and amyloid-beta aggregation. Further research especially large-scale clinical trials are warranted to strengthen the preclinical evidence. In conclusion, neurosteroids augmentation could provide a new avenue for prevention and symptomatic management in AD. In summary, this draft abstract highlights the key findings from the research review on neuroprotective roles of allopregnanolone and 24(S)-hydroxycholesterol in Alzheimer's disease models and patients. It summarizes the major outcomes demonstrating their abilities to reduce neurodegeneration, inflammation and amyloid-beta pathology. The abstract concludes that these neurosteroids represent promising novel therapeutic candidates for Alzheimer's disease worthy of further clinical investigation. Please let me know if you would like me to modify or expand the abstract in any way.