Study finds increased microglial neuronal discharges and improve brain cell survival after injury -
A type of immune cell widely believed to exacerbate adult chronic brain diseases such as Alzheimer's disease and multiple sclerosis (MS), can effectively protect the brain against traumatic brain injury (TBI) and may slow the progression of neurodegenerative diseases, according to a clinical study published in Cleveland today in the online journal Nature Communications .
The research team, led by Bruce Trapp, PhD, chair of the Department of Neurosciences at the Lerner Research Institute of Cleveland Clinic, found that microglia may help synchronize the brain fire, which protects the brain from TBI and can help relieve chronic neurological diseases. They provided the most detailed study and visual evidence of the mechanisms involved in this protection.
"Our results suggest that the innate immune system helps protect the brain after injury or during chronic diseases, and this role should be further studied," said Dr. Trapp. "We could potentially exploit the protective role of microglia to improve the prognosis of patients with TBI and delay disease progression, MS, Alzheimer's and stroke. The methods we have developed will help us further understand the mechanisms of neuroprotection. "
Microglias are primary responders to the brain after an injury or sickness. Although researchers have long believed that activated microglia causes harmful inflammation that destroys healthy brain cells, some speculate a more protective role. The team of Dr. Trapp used an advanced technique called 3D electron microscopy to visualize the activation of microglia and subsequent events in animal models.
They found that when chemically activated, microglia migrate to inhibitory synapses, the connections between brain cells that slow firing pulses. They displace the synapse (called "stripping synaptic"), thereby increasing neuronal firing, leading to a cascade of events that improve the survival of brain cells.
Trapp is internationally known for his work on the mechanisms of neurodegeneration and repair in multiple sclerosis. His research has included investigating the cause of neurological disability in patients with multiple sclerosis, the cellular mechanisms of brain repair in neurodegenerative diseases and molecular biology of myelination in the central and peripheral nervous systems.
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