Abstract: Higher prevalence of sporadic Alzheimer’s disease in women: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder caused by the accumulation of amyloid-β (Aβ) plaques and Tau neurofibrillary tangles in the affected brain regions. The clearance of these pathological protein aggregates by microglia can trigger excessive neuroinflammation, which contributes to brain atrophy. AD exhibits clinical heterogeneity and is characterized by highly complex, multifactorial etiology (Lopez-Lee et al., 2024). In the rare autosomal dominant forms of familial AD, patients inherit mutations in genes encoding amyloid precursor protein or presenilins. In contrast, the majority of the cases are classified as late-onset sporadic AD, in which aging is the primary risk factor. Disease susceptibility is sexbiased, with approximately 1 in 5 women at risk of developing AD during their lifetime, compared to 1 in 10 men. Beyond socio-cultural factors, a previous study suggests that inherent biological differences between the sexes contribute to the higher prevalence of AD in women (Lopez-Lee et al., 2024). For example, hormonal fluctuations during menopause can disrupt metabolic and inflammatory processes, increasing vulnerability to AD. Sex-specific differences in gene regulation and autophagy may also significantly impair protein homeostasis in females, thereby exacerbating AD pathology. Identifying other sex-biased mechanisms will deepen our understanding of AD etiology and lead to more effective treatment.