Carefully Targeting Brain Immune Cells May Help Prevent Amyloid-beta Plaques, Study Suggests

Carefully Targeting Brain Immune Cells May Help Prevent Amyloid-beta Plaques, Study Suggests
Therapeutics that target brain immune cells known as microglia may prevent the formation of amyloid-beta plaques, one of the hallmarks of Alzheimer’s disease, according to a recent mouse study. The study, ”Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model," was published in the journal Nature Communications. Alzheimer’s disease is characterized by the formation of amyloid-beta protein aggregates (plaques) that accumulate between nerve cells in the brain, disrupting their function. Microglia, the immune cells of the central nervous system (brain and spinal cord), are responsible for maintaining cell balance within the brain. They release pro- and anti-inflammatory signals in response to changes in the brain’s microenvironment, clearing amyloid-beta aggregates in the brain and contributing to the health of the brain’s neuronal network. Microglia have been implicated in Alzheimer’s disease. Research has shown that removal of microglia from mouse models of Alzheimer’s during the advanced stages of the disease — when there is an extensive build-up of amyloid-beta plaques — protected against the loss of neurons and synapses (the junctions between two nerve cells that allow them to communicate). Furthermore, most of the genes associated with an increased risk of developing Alzheimer’s are active in microglia. Despite this evidence, the exact
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