Cell: Chen Wei/Lu Yi, etc. reveals how the brain copes with Alzheimer's amyloid deposition plaques?

!---- Ancient Greek and Roman philosophers discovered the ageing-related dementia until 1901, when Dr. Alois Alzheimer reported on the symptoms of a 55-year-old patient and the massive accumulation of amyloid plaques in his brain after his death, which was named Alzheimer's disease.a century, many scientists have tried to piece together pathological changes in the brain by describing lesions of different molecules or cells in the face of amyloid plaques from different angles.however, the brain structure is quite complex, and there are many different cell types and functions in tens of billions of cells.focus on changes in a cell or molecule are often invisible to the tree, and it is not possible to understand the whole picture how different cells work and interact with starch-like plaques.scientists still have a clear relationship between these starchy plaques and the course of the disease., 22 July 2020, Professor Bart De Strooper of the Frams Institute of Biotechnology (VIB) and the University of Leuven, Belgium, and Bioinformatics, Dr. Mark Fiers(Co-Elongati) A study published in Cell on Spatial rulomics and in situ dating to study Alzheimer's Disease reveals complex neurodegenerative mechanisms in which beta-amyloid deposits may act as "triggers" or "drivers" in the course of disease, triggering multicellular synergies.the study uses the latest technology - spatial transcription groups - to systematically define the multicellular gene regulation network (multicellular gene regulatory network) caused by amyloid plaques, which consists of 57 transcripts and is named Plaque-Induced Genes (PIGs).the study found no synergy in the brains of normal mice, however, with the accumulation of beta-amyloid, 57 PIGs gradually constructed a regulatory network dominated by astrocytes and nerve gum cells (see figure below).this network symbolizes the activation of the complement system through the classical pathway and the abnormality of the lysosomal pathway., the study also found another regulatory network dominated by oligoscotatose cells, which is stimulated by the accumulation of small amounts of beta-amyloid protein but depleted when high-intensity beta-amyloid protein accumulates. Professor de Strooper,, said: "Our study shows that amyloid plaques are not a by-product of 'innocent' disease, but rather trigger triggers strong synergies in multiple cells.further research is needed in the future to see if removing amyloid plaques can effectively reverse the pathological machine rotation of these cells."