A single-cell atlas of the aging mouse ovary reveals significant changes in ovarian cell composition and function with age. In young (3-month-old) and reproductively aged (9-month-old) mice, the proportion of immune cells in the ovary doubles, with lymphocytes increasing the most. This is confirmed by flow cytometry. Age-related downregulation of collagenase pathways in stromal fibroblasts is associated with increased ovarian fibrosis. Follicular cells show increased stress-response, immunogenic, and fibrotic signaling. The study provides insights into the mechanisms of ovarian aging, including immune cell accumulation, fibrosis, and changes in the ovarian microenvironment. The data are available via a Shiny-based web application. Ovarian aging is linked to reduced fertility, dysregulated endocrine signaling, and increased chronic disease burden. As the ovary ages, the local microenvironment changes, reducing oocyte quality and increasing follicular depletion, leading to menopause. Menopause is associated with accelerated systemic aging, increased chronic disease burden, and higher all-cause mortality risk. Understanding the mechanisms of ovarian aging is crucial for extending female fertility and reducing age-related chronic disease. Age-related ovarian follicular depletion is associated with mitochondrial dysfunction, reactive oxygen species production, inflammation, and fibrosis. However, the specific cell types contributing to these phenotypes are not well understood. Recent studies have focused on the role of ovarian stromal cells in ovarian health and disease. The study shows that markers of cellular senescence and fibrogenesis increase in the ovarian stroma with age, although the specific cell types remain unknown. Multinucleated giant cells (MNGCs) accumulate with age, potentially contributing to the aforementioned phenotypes. Due to the dynamic nature of ovarian function, it has been challenging to identify the cell type-specific mechanisms underlying follicular depletion and ovarian failure. Single-cell analyses of ovarian aging in nonhuman primates and humans are ongoing. Mice are the most commonly used model organism for ovarian aging studies due to their short lifespan and ease of genetic manipulation. A previous study identified age-related changes in ovarian cell populations, but lacked the resolution to identify specific cellular subtypes and immune populations. This study used single-cell RNA sequencing (scRNA-seq) to identify age-related transcriptional changes in a cell type-specific manner within the mouse ovary at 3 and 9 months of age. The study found that the percentage of granulosa cells (GCs) was lower in 9-month-old ovaries, which can be explained by declines in the number of primordial and tertiary follicles and a trending decline in secondary follicles. The most marked change in ovarian cellularity with advancing age was the greater than twofold increase in immune cells. The study also found that the proportion of CD4+ T cells increased in the aged ovary. However, neither natural killer (NK) cells nor ILC2s were significantly changedA single-cell atlas of the aging mouse ovary reveals significant changes in ovarian cell composition and function with age. In young (3-month-old) and reproductively aged (9-month-old) mice, the proportion of immune cells in the ovary doubles, with lymphocytes increasing the most. This is confirmed by flow cytometry. Age-related downregulation of collagenase pathways in stromal fibroblasts is associated with increased ovarian fibrosis. Follicular cells show increased stress-response, immunogenic, and fibrotic signaling. The study provides insights into the mechanisms of ovarian aging, including immune cell accumulation, fibrosis, and changes in the ovarian microenvironment. The data are available via a Shiny-based web application. Ovarian aging is linked to reduced fertility, dysregulated endocrine signaling, and increased chronic disease burden. As the ovary ages, the local microenvironment changes, reducing oocyte quality and increasing follicular depletion, leading to menopause. Menopause is associated with accelerated systemic aging, increased chronic disease burden, and higher all-cause mortality risk. Understanding the mechanisms of ovarian aging is crucial for extending female fertility and reducing age-related chronic disease. Age-related ovarian follicular depletion is associated with mitochondrial dysfunction, reactive oxygen species production, inflammation, and fibrosis. However, the specific cell types contributing to these phenotypes are not well understood. Recent studies have focused on the role of ovarian stromal cells in ovarian health and disease. The study shows that markers of cellular senescence and fibrogenesis increase in the ovarian stroma with age, although the specific cell types remain unknown. Multinucleated giant cells (MNGCs) accumulate with age, potentially contributing to the aforementioned phenotypes. Due to the dynamic nature of ovarian function, it has been challenging to identify the cell type-specific mechanisms underlying follicular depletion and ovarian failure. Single-cell analyses of ovarian aging in nonhuman primates and humans are ongoing. Mice are the most commonly used model organism for ovarian aging studies due to their short lifespan and ease of genetic manipulation. A previous study identified age-related changes in ovarian cell populations, but lacked the resolution to identify specific cellular subtypes and immune populations. This study used single-cell RNA sequencing (scRNA-seq) to identify age-related transcriptional changes in a cell type-specific manner within the mouse ovary at 3 and 9 months of age. The study found that the percentage of granulosa cells (GCs) was lower in 9-month-old ovaries, which can be explained by declines in the number of primordial and tertiary follicles and a trending decline in secondary follicles. The most marked change in ovarian cellularity with advancing age was the greater than twofold increase in immune cells. The study also found that the proportion of CD4+ T cells increased in the aged ovary. However, neither natural killer (NK) cells nor ILC2s were significantly changed