Alzheimer’s disease is the most common form of dementia and is characterized by neurodegeneration of areas of the brain involved in memory and learning. Amyloid beta and tau are two toxic proteins that accumulate in disease and ultimately cause neuronal cell death, but little is known about how other cells in the brain react during the course of the disease. not.
A new study by the ASU-Banner Neurodegeneration Research Center (NDRC) and the MIT / Koch Institute sheds new light on how the disease process manifests itself in patients with Alzheimer’s disease.
Diego Mastroeni of the NDRC worked with MIT colleagues in the Department of Biological Engineering Forest White and Douglas Lauffenburger to investigate how proteins and signaling pathways in patients with Alzheimer’s disease change.Their analysis captures a detailed molecular profile of changes known as changes at the protein level. Protein phosphorylation An entire cohort of patients with well-preserved brain tissue by the Banner Sun Health Research Institute. Their work takes advantage of the heterogeneity inherent in human research to create new models of disease progression.
“This manuscript emphasizes the importance of integrating the phosphoproteome with the proteome and transcriptome datasets to obtain better images of the disease driver, from transcription to translation,” said Mastroni. I will. (A phosphoproteome is a protein that has undergone epigenetic modification by the addition of a phosphate group. The proteome contains the complete complement of all proteins in the body, and the transcriptome is gene-generated. Refers to an RNA message, which is then converted to a protein.)
Researchers’ analysis shows toxic protein accumulation, neurodegeneration, and Glial cells Supports and protects neurons in the brain. In particular, they found an interesting association between markers of neurodegeneration and two types of glial cells, oligodendrocytes and microglia. Progressive changes in these cells may be key to understanding the causes of neurodegeneration.
New study published in journal Natural aging..
Our results show that there are many cellular signaling pathways that are activated at all stages of the disease. It may be possible to reuse available therapies to target protein kinases that regulate these cell signaling events. Clinicians today are studying the therapeutic effects on amyloid and tau on behalf of the disease, but our results suggest that glial cells are involved in every step of the process. A better understanding of glial cells and their role in progressive neurodegeneration may open up new opportunities for the treatment of this disease. “
Forest White, MIT Department of Biological Engineering
“This collaboration is like what we do with the NDRC values,” says Mastroeni. “No one can tackle the disease on their own. It will take group efforts to combat this catastrophic disease.”
Mosheed, N. , Et al. (2021) Quantitative phosphoproteomics reveals a dysregulated kinase network in Alzheimer’s disease. Nature aging. doi.org/10.1038/s43587-021-00071-1..
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