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

When Dr. Alois Alzheimer first described lesions in the brain more than 100 years ago, he did not think that until now, the origin of the disease, named after his name, had not been clear.
problems are focused on a pathological phenomenon called amyloid protein deposition.
in Dr. Alzheimer's's case description, a young dementia patient has a deposit of amyloid protein in his brain. After
, it was also attributed to one of the typical pathological changes in Alzheimer's disease.
however, there has been much debate about the specific impact of this lesions.
at 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 them.
However, several clinical trials have failed in more than a decade, raising doubts about the specific function of amyloid protein.
some scientists have suggested that it may be just a pathological manifestation of Alzheimer's disease and have no direct effect on the onset of the disease.
corresponding, attention is diverted to inflammation and assumptions about viral infections, or bacterial infections.
and whether or not these assumptions are accurate.
a paper published online today in the journal Cell, suggests that perhaps we shouldn't ignore amyloid deposits and simply think it's just a product of disease.
, on the contrary, it may still promote the onset of Alzheimer's disease.
This 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 tissues with a diameter of 100 microns near the diseased amyloid deposits as an analysis of transcription groups.
interesting, they observed changes in the gene-co-expression network of some of these tissues.
these changes occur mainly in the supporting cells of the two brains, astrocytes and small glial cells.
this multigene change does not occur when there is no amyloid protein deposition.
, the scientists observed a network of common expressions of genes, which occur mainly in small-protrusion cells.
the network is activated when amyloid protein deposits are not severe.
these changes disappear when amyloid protein deposits are severe.
these genes, which are activated by amyloid induction, are mainly involved in physiological processes such as supplementary system, oxidative stress, lysozye function, and inflammatory metabolism.
using in-situ sequencing techniques, scientists validated these observations at cell levels in brain slices in mice and humans.
the results 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 deposition may trigger, or drive disease.
deposition in the brain, it can trigger a complex multicellular neurodegenerative process.
" said Professor Bart De Strooper, one of the study's authors.
the authors point out that we should further study the effects of amyloid protein deposits on Alzheimer's disease.
we have to answer the question of whether removing these deposits "does" help reverse the process of cell lesions.
we also need to answer the question of "when" to clear it to effectively reverse the condition.
in addition, we will look at whether the current antibodies against amyloid deposits can really reverse the corresponding gene-based expression network.
this may explain why most past clinical trials have failed - you know, different antibodies can produce very different effects.
References: Wei-Ting Chen et al., (2020), Spatial R. R. And In Situing to Study's Disease, Cell, DOI: What happens around an Alzheimer?? Retrieved July 22, 2020, from.