"Investigators from the laboratory of Puneet Opal, MD, '95 PhD, the Lewis John Pollock Professor of Neurology in the Division of Movement Disorders and of Cell and Developmental Biology, who was senior author of the study, employed a combination of genetic and RNA interference (RNAi) approaches to study the brains of mice which lacked gigaxonin."
"They observed that the cellular recycling processes were disrupted because the neurofilaments acted like Velcro in the brain, preventing organelles from moving, according to the study. Additionally, the cellular recycling plants - called lysosomes - were missing key digestive enzymes responsible for breaking down waste products, the scientists found."
""These vesicles can't reach the garbage can - lysosomes," Opal said. "So, the neurofilaments cannot be degraded by that. Additionally, the neurofilaments create docking sites for proteins and organelles normally, but in the disease, these sites are a little bit garbled.""
Genetic and RNA interference approaches in gigaxonin-deficient mice revealed neurofilament aggregation that behaves like Velcro, physically trapping organelles and blocking their movement. Cellular recycling pathways became disrupted as organelle-containing vesicles failed to reach lysosomes. Lysosomes lacked key digestive enzymes required to degrade waste, preventing neurofilament turnover. Neurofilaments normally provide docking sites for proteins and organelles, but in the diseased state those sites became disorganized and dysfunctional. Immunofluorescence of dorsal root ganglia from Gan null mice showed prominent neurofilament aggregates in neurons, with satellite glial cells stained by GFAP and nuclei counterstained by DAPI.
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