Microglial galectin-3 increases with aging in the mouse hippocampus.

Hyun Joo Shin, So Jeong Lee, Hyeong Seok An, Ha Nyeoung Choi, Eun Ae Jeong, Jaewoong Lee, Kyung Eun Kim, Bong-Hoi Choi, Seung Pil Yun, Dawon Kang, Sang Soo Kang, Gu Seob Roh

Department of Anatomy and Convergence Medical Science, Institute of Medical Science, College of Medicine, Gyeongsang National University, Jinju 52727, Korea. · pubmed

Paper

Abstract

Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of galectin-3 in microglial activation and neuroinflammation during brain aging, which is relevant to understanding mechanisms of aging and potential interventions. However, the findings appear to be incremental and primarily descriptive, focusing on the correlation of galectin-3 with aging rather than addressing root causes or proposing solutions for lifespan extension or age-related diseases. Thus, while it contributes to the field, its impact is limited.

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