Senescence-related Stress Responses in Immuno and Neurological Aging

In recent years, the discovery of several novel senescence-related immune and neurological responses has attracted significant attention. The stress associated with mitochondrial protein folding is a driver of neural stem cell aging and suggests approaches to ameliorate aging-associated cognitive decline. In other breakthroughs, targeting bone marrow-derived senescent immune cells offers an avenue for improving brown adipose tissue aging and related metabolic disorders. Research also reveals the protective role of microglial autophagy in regulating the homeostasis of amyloid plaques and in preventing senescence; thus, the removal of senescent microglia emerges as a promising therapeutic strategy.

The mitochondrial unfolded protein response regulates hippocampal neural stem cell aging
Click here for the original article: Chih-Ling Wang , et. al., Cell Metabolism, 2023.

Senescent immune cells accumulation promotes brown adipose tissue dysfunction during aging
Click here for the original article: Xu Feng, et. al., Nature Communications, 2023.

Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence
Click here for the original article: Insup Choi , et. al., Nature Cell Biology, 2023.

Point of Interest
- Mitochondrial protein-folding stress increases in neural stem cells as they age.
- SIRT7 protects neural stem cells by reducing mitochondrial protein-folding stress.
- Overexpression of SIRT7 enhances neurogenesis and improves cognition in aged mice.

Point of Interest
- Senescent immune cells, predominantly T cells and neutrophils, secrete an abundance of S100A8.
- These S100A8-expressing immune cells, in conjunction with adipocytes and sympathetic nerves, lead to a reduction in thermogenic function.
- An S100A8 inhibitor rejuvenates the axon networks within brown adipose tissue and restores thermogenic function in aged male mice.

Point of Interest
- Inhibiting microglial autophagy leads to the disengagement of microglia from amyloid plaques, exacerbating neuropathology in mice with Alzheimer's Disease (AD).
- An autophagy deficiency fosters the development of senescent microglia.
- Pharmacological removal of autophagy-deficient senescent microglia can alleviate neuropathology in mice with AD.

Metabolic shift to glycolysis in senescenct cells

NAD(+) levels decline during the aging process, causing defects in nuclear and mitochondrial functions and resulting in many age-associated pathologies*. Here, we try to redemonstrate this phenomenon in the doxorubicin (DOX)-induced cellular senescence model with a comprehensive analysis of our products.

*S. Imai, et al., Trends Cell Biol, 2014, 24, 464-471

Products in Use
① DNA Damage Detection Kit - γH2AX
② Cellular Senescence Detection Kit - SPiDER-βGal
③ NAD/NADH Assay Kit-WST
④ JC-1 MitoMP Detection Kit
⑤ Glycolysis/OXPHOS Assay Kit、Lactate Assay Kit-WST