Now reverse? Cell revisits the role of important pathological proteins in Alzheimer's disease.

The problem is focused on a pathological phenomenon called amyloid protein depositionIn DrAlzheimer's's case description, a young dementia patient has a deposit of amyloid protein in his brainIt was then attributed to one of the typical pathological changes in Alzheimer's diseaseHowever, there has been much debate about the specific impact of this lesionsAt first, amyloid protein deposits were thought to be the cause of Alzheimer's disease, and much scientific research has been devoted to how to remove these lesions and reverse themHowever, several clinical trials have failed for more than a decade, raising questions about the specific function of amyloid proteinSome scientists have also suggested that it may be just a pathological manifestation of Alzheimer's disease and have no direct effect on the onset of the diseaseCorrespondingly, attention is diverted to inflammation and assumptions about viral infections, or bacterial infectionsAnd whether or not these assumptions are accurateIn a paper published online today in the journal Cell, it is suggesting that perhaps we should not ignore amyloid deposits and simply assume that it is simply a product of diseaseOn the contrary, it may still promote the onset of Alzheimer's diseasethis study helped us re-understand the role of amyloid protein deposition (Photo: NIH Image Gallery from Bethesda, Maryland, USA / Public Domain) In this study, researchers used mouse models of Alzheimer's disease to extract peripheral tissue sized 100 microns in diameter near the diseased amyloid protein deposits for analysis of transcription groupsInterestingly, they observed changes in the gene-co-expression network of some of these tissuesThese changes occur mainly in the supporting cells of the two brains, astrocytes and small glial cellsThis multigene change does not occur when amyloid protein is not depositedIn addition, the scientists observed a network of common expressions of another gene, which is mainly found in small-protrusion cellsThis network is activated when amyloid protein deposits are not severeWhen amyloid protein deposits are severe, these changes disappearThese genes, activated by amyloid induction, are mainly involved in physiological processes such as supplementation system, oxidative stress, lysozye function, and inflammatory metabolismUsing in-situ sequencing techniques, scientists validated these observations at the cellular level in brain slices of mice and humansthe illustrations of this study (Photo Source: References) These results clearly show that amyloid protein deposition is not a simple "pathogenia" but rather a series of genetic changes that may be involved in the onset of neurodegenerative diseases"Amyloid protein deposits may trigger, or drive diseaseDeposition in the brain may initiate a complex multicellular neurodegenerative processProfessor Bart De Strooper, one of the study's authors, saidThe authors point out that we should further study the effects of amyloid protein deposits on Alzheimer's diseaseNot only do we have to answer the question of whether removing these deposits , "whether" it helps reverse the process of cell lesionsWe also need to answer the question of "when" to clear the disease to effectively reverse the conditionIn addition, we will look at whether the current antibodies against amyloid deposits can really reverse the corresponding gene-based expression networkThis may explain why most past clinical trials have failed - you know, different antibodies can produce very different effectsReferences: Wei-Ting Chen et al., (2020), Spatial Rats and In Situing to Alzheimer's Disease, Cell, DOI: s2? Retrieved July 22, 2020, from