Background: Alzheimer’s disease (AD), a progressive neurological disease, affects millions of individuals globally, with a disproportionately high impact on women. Changes in the gut microbiota through the gut‒brain axis have been connected to AD pathogenesis in recent studies. However, few studies have investigated how sex-specific variations in gut microbiota diversity and composition are related to AD. This study explores these variations and their possible effects on the course of the disease and the development of new treatments. Methods: This study explored publicly available 16S RNA amplicon sequencing data obtained from a clinical experiment conducted on US patients with AD. In that experiment, a total of 14 fecal samples were obtained from both male and female AD patients and were compared with 14 control samples. High-throughput 16S rRNA sequencing was subsequently performed. We conducted an analysis of the bacterial communities at the phylum, genus, and species levels via taxonomic profiling via the EzBioCloud workflow. Microbial richness and diversity within individual samples were evaluated via alpha diversity metrics. To assess variations in microbial composition between sexes, beta diversity analysis utilizing Bray‒Curtis dissimilarity was used. To identify notable variations in particular taxa and their relative abundances, comparative studies were conducted. Results: The gut microbiota of AD patients clearly presented sex-specific variations, according to the present study. A median Shannon index of 3.9 for females and 3.7 for males was associated with significantly greater alpha diversity. Similarly, females presented greater microbial richness according to the Chao1 index. Beneficial bacterial taxa such as Akkermansia muciniphila and other genera that produce short-chain fatty acids (SCFAs), which are linked to anti-inflammatory and neuroprotective qualities, were more abundant in females. On the other hand, pro-inflammatory taxa, such as Ruminococcus faecis, which are connected to systemic inflammation and may exacerbate neurodegeneration, were more prevalent in males. The impact of sex on the composition of the gut microbiota was further highlighted by beta diversity analysis, which also revealed unique microbial communities clumping between sexes. Conclusions: The results highlight how important sex-specific variations in the gut microbiota are in determining the pathophysiology of AD. Males present a proinflammatory microbial environment that exacerbates AD pathogenesis, whereas females present a more varied and neuroprotective gut microbiota profile that might slow the progression of the illness. These findings emphasize how crucial it is to incorporate sex concerns into AD research and treatment planning. Given the distinct microbial profiles of males and females, personalized, microbiome-targeted therapy, such as dietary changes and probiotics, may be effective ways to reduce the risk and progression of AD. To better understand the functional consequences of these findings and maximize therapeutic therapies, future research should concentrate on multi-omics techniques and larger, longitudinal investigations.