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Multiple sclerosis (MS)-associated inflammation in the cerebral cortex the outermost layer of the brain that is involved in cognitive function prompts the destruction of neural connections by specific immune cells, according to a study in a mouse model of MS.
These immune cells targeted dendritic spines (nerve cell communication structures) containing abnormally high levels of calcium a dysregulation previously associated with nerve fiber degeneration in MS.
Importantly, blocking the activation of these immune cells, called phagocytes, successfully prevented the loss of cerebral cortex synapses (sites of neural communication) in the mice, highlighting that similar approaches may help prevent disease progression in people with MS.
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Immune cells attack synapses
Damage to the brain gray matter plays an important role in the progression of multiple sclerosis. A team of neuroscientists has now shown that the cause are inflammatory responses that lead to synapse loss, reducing neuronal activity. Targeted inhibition of these immune cells could mitigate such synaptic damage, and therefore provides a promising therapeutic option for progressive multiple sclerosis.
Multiple sclerosis (MS) is a chronic inflammatory disease that affects the central nervous system, in which nerve cells are attacked by the patient’s own immune system. In many cases, the disease develops into a progressive form, which is characterized by a shift of pathology from the white matter to the gray matter, for instance to the cerebral cortex. This phase of the disease has so far been difficult to treat and its underlying causes are poorly understood.
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Damage to the brain gray matter plays an important role in the progression of multiple sclerosis. This study now shows that such damage can be caused by inflammatory reactions that lead to loss of synapses, which impairs neural activity.
Multiple sclerosis (MS) is a chronic inflammatory disease that affects the central nervous system, in which nerve cells are attacked by the patient s own immune system. In many cases, the disease develops into a progressive form, which is characterized by a shift of pathology from the white matter to the gray matter, for instance to the cerebral cortex. This phase of the disease has so far been difficult to treat and its underlying causes are poorly understood. Now, a research team led by Martin Kerschensteiner, Director of the Institute for Clinical Neuroimmunology at LMU, in cooperation with Thomas Misgeld (Technical University of Munich) and Doron Merkler (University of Geneva), has shown in a mouse model that inflammation of the gray m