Researchers at the University of Colorado School of Medicine have identified how specific brain cells interacting during development could be related to neurological and neuropsychiatric diseases, including some that occur later in life.
Brain function depends on the precise formation of millions of connections between specific brain cell types, including neurons and glial cells. The scientists at CU studied how a type of connection, called myelination, functions between specific cell types and how the body’s nervous system removes excess connections. Details of their research are outlined in an article published Monday, July 6, in the journal Nature Neuroscience.
“We believe these new data will lead to improved understanding of the potential causes for some neurological and neuropsychiatric diseases,” said senior author Bruce Appel, PhD, professor and head of the Department of Pediatrics Section of Developmental Biology.
Appel and first author Alexandria N. Hughes, a graduate student in the CU Graduate School’s Neuroscience Program, used larval zebrafish, small and transparent vertebrates that share many aspects of nervous system development with humans. Because zebrafish larvae are transparent, cells of the nervous system can be watched during the course of development.
The team found that microglia, which are the brain’s population of immune cells that defend against infection throughout life, also play an essential role in regulating myelination. Myelination is a connection process formed between electrically active neurons and a glial cell type called oligodendrocytes. Oligodendrocytes wrap the long axons of neurons with segments of fatty myelin membrane to insulate them, which increases the speed brain signals are sent.
The process of how the nervous system removes incorrect myelin segments, or sheaths, is unknown.
In their study, the CU researchers observed that microglia extend within myelinated tracts of the nervous system and examine individual myelin sheaths, removing some of them by phagocytosis, or cellular “eating.” Furthermore, the amount of myelin that microglia ate depended on neuronal activity, suggesting that microglia may listen to neurons to determine whether to remove myelin.
Understanding myelin is important because myelin abnormalities are a hallmark of numerous neurological and neuropsychiatric diseases, including Alzheimer’s disease, schizophrenia, and autism spectrum disorder….
Well gee, vaccines are all about “tweaking” the immune system with a ball peen hammer. Maybe they can invent an anti-autism vaccine!
Medicine’s capacity to ignore what is right in front of them is a wonder to behold.
Reactivity to myelin antigens in multiple sclerosis. Peripheral blood lymphocytes respond predominantly to myelin oligodendrocyte glycoprotein.
Although T cell responses to the quantitatively major myelin proteins, myelin basic protein (MBP) and proteolipid protein (PLP), are likely to be of importance in the course of multiple sclerosis (MS), cell-mediated autoimmune responses to other myelin antigens, in particular quantitatively minor myelin antigens, such as myelin-associated glycoprotein (MAG) and the central nervous system-specific myelin oligodendrocyte glycoprotein (MOG), could also play a prevalent role in disease initiation or progression. Highly purified myelin antigens were used in this study to assess cell-mediated immune response to MOG in MS patients, in the context of the reactivity to other myelin antigens, MBP, PLP, and MAG. The greatest incidence of proliferative response by MS peripheral blood lymphocytes was to MOG, as 12 of 24 patients tested reacted and, of these, 8 reacted to MOG exclusively. In contrast, only 1 control individual of 16 tested reacted positively to MOG. The incidence of responses to MBP, PLP, and MAG did not differ greatly between MS patients and control individuals. A predominant T cell reactivity to MOG in MS suggests an important role for cell-mediated immune response to this antigen in the pathogenesis of MS.