Astrocytes, brain cells thought to migrate to and destroy the amyloid plaques that are associated with the development of Alzheimer’s disease, are actually repelled by the plaques, researchers analyzing models of the brain report. Their study, titled “Topological analyses in APP/PS1 mice reveal that astrocytes do not migrate to amyloid-β plaques,” was recently published in Proceedings of the National Academy of Sciences (PNAS).
Astrocytes, the most abundant cell type in the central nervous system, are involved in the structural and metabolic support of neurons and the stability of synaptic activity. Several studies have suggested that amyloid plaques, a hallmark of Alzheimer’s disease pathogenicity, attract these cells to reduce the presence of amyloid structures and alleviate injury. This mechanism, in fact, has been explored in the ongoing development of new therapeutic strategies for AD, but more recent research suggests that astrocyte migration does not occur following injury.
To re-examine astrocyte reaction to amyloid plaques, researchers from the Institute of Neuroscience of the Universitat Autònoma de Barcelona, in collaboration with Massachusetts General Hospital, studied astrocyte distribution in the brains of Alzheimer’s mouse models, applying quantitative spatial analysis and computer modeling used in physics studies.
By examining 3-D images of astrocyte distribution, researchers observed these cells repel each other and are repelled by amyloid plaques. This balance of repulsive forces maintains the territorial organization of astrocytes and, contrary the previous AD research, astrocytes do not break this organization to migrate to and phagocytose plaques. The response to the presence of pathogenic plaques is observed through the up-regulation of these cells’ key molecule, glial fibrillary acidic protein (GFAP), suggesting that astrocytes do react to this pathogenicity, but in a different way than previously thought. Such observations led researchers to conclude that astrocytes respond to plaque formation not by changing position but by modifying their function.
Dr. Elena Galea, one of the paper’s authors, said in a press release, “This discovery is very important, as the elimination of amyloid plaques by the brain cells themselves is one of the key strategies under development as a cure for Alzheimer’s disease. Therefore, clarifying which cells can and cannot eliminate the plaques is essential for obtaining effective therapies.”
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