Topic: lysosomal dysfunction

Mucopolysaccharidosis IIIA (MPS-IIIA) is a severe inborn error of metabolism caused by mutations in the sulfamidase gene (SGSH), which encodes a lysosomal enzyme involved in the metabolism of heparan sulfate (HS). Defective sulfamidase activity leads to the accumulation of HS within lysosomes, resulting in lysosomal dysfunction and ultimately leading to neurodegeneration and dementia in affected children. However, preceding dementia, individuals often exhibit severe and debilitating autistic-like behaviors, including self-injury, stereotypic behaviors, and social impairment. These autistic sym

Our environment is polluted with plastic waste, wherein the degradation leads to the formation of micro and nanoplastics (NPs). These plastic particles contaminate water, soil, air, and food, exposing humans throughout their lives. Although NPs are detected in the human body, such as in blood, feces, and placenta, their potential impact on human health remains poorly understood. Moreover, the developing brains of fetuses and children may be sensitive to these molecules, potentially leading to functional impairments and altered behavior. Our study investigates the impact of chronic, low-dose ex

Microglia, as macrophages in the brain, exhibit dysfunction with aging, such as impaired phagocytic capability and elevated neuroinflammation. However, the mechanisms underlying microglial aging remain unclear. The heterogeneity of microglia further challenges this context. Disrupted-in-schizophrenia 1 (DISC1), a psychiatric disorder susceptibility gene disrupted by translocation, plays an essential role in regulating the development and function of neurons. We observe that DISC1 is also expressed in microglia, where it exhibits an aggregates-like pattern (Figure A). We called this population