News Damage to Nerve Synapses in MS Mouse Model Found to Be Unrelated to Myelin Destruction Damage to Nerve Synapses in MS Mouse Model Found to Be Unrelated to Myelin Destruction by Patricia Silva, PhD | March 9, 2016 Share this article: Share article via email Copy article link ResearchersĀ found that nerve cell connections in the brain, called synapses, wereĀ damaged in aĀ mouse model ofĀ multiple sclerosis (MS) through a process wholly unrelated toĀ myelin destruction. As the damaged mice synapses studied were inĀ regions crucial for memory processing, findingĀ ways of protecting these neurons would be a crucial step toward developing a treatment that preserves cognitive function in MS patients. The studyĀ ā published in the Journal of Neuroscience under the title “Platelet-Activating Factor Receptors Mediate Excitatory Postsynaptic Hippocampal Injury in Experimental Autoimmune Encephalomyelitis“Ā ā gives scientists entirely new insights into processes of nerve damage affecting MS patients. In previous research, scientists observed that damage to the brain’s gray matter ā areas holding densely packed unmyelinated nerve cell bodies ā occur without correlation to myelin destruction. In MS, damage to these neurons occur in areas that are important for cognition, thereby contributing to disability. Scientists, however, know little about the mechanisms behind damage to these nerve cells. Because of this, attempts to develop therapies that might protect the neurons from damage so as to slow or stop the disease’s progressive disability are still in their infancy. The team, led byĀ Matthew BellizziĀ and Harris GelbardĀ at the University of Rochester Medical Center,Ā studied mice with experimental autoimmune encephalopathy (EAE), used to model MS. They focused on the hippocampus, a brain region crucial for the processing of memories, particularly spatial memory, and the process of consolidatingĀ short-term memories into long-term ones. When researchers comparedĀ the density of synapses in the EAE mice to normal mice, they saw that the MS-like mice had a 28 percent reduction in synaptic density, despite intact myelin. The team also noted that activated microglial cells were presentĀ at the same sites where scientists found synaptic debris. Microglia are the brain’s main type of immune cell, and when activated they are known to produce substances that can be toxic to neurons. To determineĀ if the presence of microglia contributed to the damage, researchersĀ then cultured neurons from the hippocampus in the lab. When they added activated microglia, they noted that the neuronsĀ became more vulnerable to damage. They also observedĀ that this increased sensitivity seemed to beĀ mediated by a factor calledĀ platelet-Āactivating factor receptor (PAFR). To confirm the role of PAFR, the team then blocked PAFR in the EAE mice using theĀ experimental moleculeĀ BN52021. When PAFR was blocked,Ā synapses were preserved, but other signs of disease remained. More research is now needed to find ways to protect these neurons in humans with MS. According to a news release from the National MS Society, which partly funded the study, the Rochester team next plansĀ to search for potential drug candidates based on theseĀ findings. Print This Page About the Author Patricia Silva, PhD PatrĆcia holds a PhD in medical microbiology and infectious diseases from the Leiden University Medical Center, Netherlands, and completed a postdoctoral research fellowship at the Instituto de Medicina Molecular, Lisbon, Portugal. Her work in academia was mainly focused on molecular biology and the genetic traits of infectious agents such as viruses and parasites. PatrĆcia earned several travel awards to present her work at international scientific meetings. She is a published author of several peer-reviewed science articles. Tags disability, gray matter
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