In 2001, we launched the Hokkaido Study, the first prospective birth cohort study in Japan. We are currently tracking the effects of environmental chemicals, using a life course approach. The study examines life circumstances after birth, and the longest follow-up to date is 20 years of age. We have measured prenatal exposure to dioxins, organochlorine pesticides, per- and polyfluoroalkyl substances, plasticizers such as di(2-ethylhexyl) phthalate, and bisphenol A. Our findings have mostly revealed that increased exposure to these environmental chemicals is linked to increased risk of lower birth size, effects on thyroid and steroid hormones, adipokine levels, as well as disruption of neurodevelopment, including causing asthma and respiratory symptoms. However, it should be noted that our findings also include protective or null findings, which may be due to low chemical concentrations or differences in prenatal or postnatal exposure. We would like to emphasize the importance of long-term continuation of the cohort, effective utilization of the data, and application of the results to environmental and health policies.

Tissue-resident macrophages perform indispensable functions in the development, maintenance, and repair of tissues. Microglia are the primary resident immune cells in the central nervous system (CNS), functioning as intracerebral macrophages distributed throughout the brain parenchyma. In addition to microglia, there is another, less well-characterized type of macrophage known as CNS border-associated macrophages (CAMs), and the existence of these cells has been recognized for several decades. With recent advances in research technologies, an increasing number of studies have focused on CAMs, and our understanding of them has begun to improve. In this article, we review the cellular characteristics and functions of CAMs that have been elucidated thus far, with a particular focus on the similarities and differences between CAMs and microglia.

Why and how do we age? This physiological phenomenon that we all experience remains a great mystery, largely unexplained even in this age of scientific and technological progress. Aging is a significant risk factor for numerous diseases, including cancer. However, underlying mechanisms responsible for this association remain to be elucidated. Recent findings have elucidated the significance of the accumulation of senescent cells and other inflammatory cells in organs and tissues with age, and their deleterious effects, such as the induction of inflammation in the microenvironment, as underlying factors contributing to organ dysfunction and disease development. Cellular senescence is a cellular phenomenon characterized by a permanent cessation of cell proliferation and secretion of several proinflammatory cytokines (senescence associated secretory phenotypes). Notably, the elimination of senescent cells from aging individuals has been demonstrated to alleviate age-related organ and tissue dysfunction, as well as various geriatric diseases. This review summarizes the molecular mechanisms by which senescent cells are induced and contribute to age-related diseases, as well as the technologies that ameliorate them.