The study found that Peli1 regulates the phagocytosis function of small glial cells and the new mechanism of Alzheimer's pathology

Recently, Xiao Qi Chuan, a researcher at the Key Laboratory of Oncology and Microethic environment at the Shanghai Institute of Nutrition and Health of the Chinese Academy of Sciences, published a research paper entitled Peli1 Impairs Microglial A phagocytosis through promoting C/EBP beta-lifed in PLOS Biology.
The study revealed that E3 ubiquity connective enzyme (i.e. Peli1) directly mediates C/EBP beta ubiquity modification and induces its degradation, affecting the new mechanism of small glial cells to devour β amyloid protein (Amyloid-β, A beta), providing new molecular targets for the pathological mechanisms and clinical treatment of Alzheimer's Disease(AD).
AD is a common neurodegenerative disease characterized by pathological changes such as A-beta deposition in the brain, resulting in neuron death and cognitive impairment.
in the Central Nervous System (CNS), the removal of A-beta depends primarily on the phagocytostic effects of small glial cells on it.
, the molecular regulatory mechanism that affects and regulates the phagocytostic function of small glial cells is not very clear.
previous studies, researchers have found that Peli1 is highly expressive in small glial cells and mediates the development and development of autoimmune neuroinflammitis, Parkinson's Disease, PD, and viral encephalitis.
the study further clarifies the pathological mechanisms in Peli1AD that negatively regulate the phagocytosis of A-beta by small glial cells, preventing the removal of A-beta deposits in the brain and worsening AD's condition.
studies show that Peli1 directly binds to and mediates the ubibinization and degradation of transcription factor C/EBP beta, and since C/EBP beta is the key transcription factor of Scavenger's subject CD36, Peli1 knocks out to promote the expression of CD36 gene and enhance the phagocytocination of small glial cells on A beta.
refore, in the brains of mice with a 5×FAD genetically modified AD model missing from the Peli1 gene in old age, the removal of A-beta by small glial cells significantly enhanced, inhibiting the deposition of A-beta in the brain.
In addition, in 5×FAD mice with small glial cells in the brain and in the brain tissue of AD patients, Peli1's expression was significantly higher than normal control, indicating that AD pathology was able to induce the expression of Peli1 in small glial cells

, Peli1 in small glial cells is a potential new molecular target for AD diagnosis and treatment.
Jing, an assistant researcher at the Institute of Nutrition and Health, and Yu Tao, a postdoctoral fellow, are co-authors of the paper, xiao Yi Chuan and Mao Chaoming of Jiangsu University Hospital are co-authors of the paper.
research has been supported by Gabriela Constantin, a professor at the University of Verona in Italy, the Institute of Nutrition and Health's public technology platform and animal platform, and has been supported by the Chinese Academy of Sciences, the Ministry of Science and Technology, the National Natural Science Foundation of China, and the Jiangsu Provincial Science and Technology Department.
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