Synaptic Loss Precedes Alzheimer’s Symptoms and Drives Disease, New Study Finds

Synaptic Loss Precedes Alzheimer’s Symptoms and Drives Disease, New Study Finds
Before any signs of cognitive decline start showing, neuronal synaptic connections are lost in mice destined to develop Alzheimer’s. New research shows that microglia – brain immune cells – destroy synapses in a fashion resembling processes in the developing brain, suggesting that it might be possible to develop drugs targeting disease at far earlier stages. The process of synaptic pruning – the loss of neuronal connections – is crucial for producing distinct neuronal circuits during normal brain development. When synapses are not successfully eliminated, conditions such as autism might arise. Excessive pruning has also been suggested to contribute to psychiatric conditions such as schizophrenia. It is easy to envision how disruption of these developmental processes might lead to disease in children and adolescents. During development, synapses are eliminated by a system relying on brain immune molecules. A protein called C1q "tags" synapses that are to be disposed of, and microglial cells get rid of the synapses by simply eating them. Researchers at Boston Children's Hospital and Harvard Medical School have now used their extensive knowledge of developmental processes to understand changes also in the aging brain – obtaining new clues of how Alzheimer’s might arise. Their study, "Complement and microglia mediate early synapse loss in Alzheimer mouse models," was recently published in the journal
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