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Researchers at the Hong Kong University of Science and Technology (HKUST) have set new treatment goals for Alzheimer’s disease by studying the brains of patients with a newly developed methodology.
This new approach also allows researchers to measure the potential effects of drugs on patients with Alzheimer’s disease, opening new directions for Alzheimer’s disease research and drug development.
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Although the pathogenic mechanisms of Alzheimer’s disease have been studied for decades, the disease is still not curable. One reason is that traditional research methods have a limited ability to define molecular targets for drug development.
Analysis of molecular pathology and pathology in general examines the brains of patients with Alzheimer’s disease as a unit, which generally reduces the contribution of different types of brain cells to Alzheimer’s disease and to its anomalies. This is particularly the case with less common cell types such as microglia (immune cells residing in the brain) and neurovascular cells (especially endothelial cells), which represent respectively less than 5% and only 1% of the total number. brain cells.
However, a team led by Professor Nancy Ibb, Vice President of Research and Development, Director of the State Key Laboratory of Molecular Neuroscience, and Professor of Life Sciences at Morningside at the Hong Kong University of Science and Technology, circumvented this problem and identified several new potential molecular targets in endothelial cells. And microglia to develop Alzheimer’s disease.
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The team examined the functions of specific types of cells in the brains of patients with Alzheimer’s disease after death, which is usually not possible with conventional methods, using evolutionary single-cell transcriptional analysis, which can be used. to characterize molecular changes in individual cells.
The analysis identified cell subtypes and pathways associated with Alzheimer’s disease, highlighting a specific subpopulation of endothelial cells found in blood vessels in the brain. As a result, the team found that increased angiogenesis (the formation of new blood vessels from existing ones) and activation of the immune system in a subset of endothelial cells correlate with disease progression. Alzheimer’s disease, indicating a link between vascular arrhythmias and Alzheimer’s disease.
The researchers also set new goals for restoring neural homeostasis (the ability to maintain a relatively stable internal state despite external changes) in patients with Alzheimer’s disease.
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The team also benefited from a single-cell transcriptome analysis to study the mechanism by which the cytokine Interleukin 33 (IL-33), an important protein for immune signaling, exerts beneficial actions, making it a potential therapeutic intervention. .
Researchers found that IL-33 reduces Alzheimer’s-like disease by stimulating the development of a specific subtype of microglia that helps clear amyloid-beta, a neuroprotein found in the brains of patients with Alzheimer’s.
They are the first to gain data on the mechanisms by which microglia transform into a phagocytic state that consumes beta-amyloid, a key cellular mechanism for eliminating pathogens.
“The complex and heterogeneous structure of brain cells makes it difficult to study disease mechanisms. Advances in single-cell technology have allowed us to identify specific subtypes of cells and molecular targets, which is essential for develop new interventions against Alzheimer’s disease, “explained Professor Ibb.
Source: medicalxpress
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