Overview
The Ultrastructure Laboratory, equipped with an Hitachi 7500 electron microscope, scanning electron microscope, ultramicrotome microscopes and other basic tools necessary for tissue processing, embedding and examination, is available for IBR researchers. They receive training and consultation to facilitate their use of laboratory equipment for their research projects.
Research conducted in the Ultrastructure Laboratory is concentrated on the detection and imaging of subcellular changes detectable only with high-resolution electron microscopy. In one study, the laboratory is expanding light microscopy studies of long-distance underconnectivity in the corpus callosum of individuals diagnosed with idiopathic and syndromic autism. The electron microscopy–based measurements of axonal diameter, axoplasm area, and myelin thickness have characterized the abnormal velocity and capacity of axonal connections between hemispheres in subjects with autism and their contribution to autism clinical deficits.
The aim of the laboratory’s second project is to determine mechanisms of infiltration by macrophage/microglia of myeloid origin of the brains of individuals diagnosed with Down syndrome and mouse models leading to capillaries’ amyloidosis, fibrillar plaque formation, and neuronal degeneration and loss of function. A parallel ultrastructural study of human brain biopsy and transgenic mice brain with amyloidosis has the potential to identify treatment that will prevent brain amyloidosis, neuronal degeneration in the third decade, and dementia in the fourth decade of life of individuals with Down Syndrome.
Research Projects
Research conducted in the Ultrastructure Laboratory is concentrated on the detection and imaging of subcellular changes detectable only with high-resolution electron microscopy.
In one study, the laboratory is expanding light microscopy studies of long-distance underconnectivity in the corpus callosum of people diagnosed with idiopathic and syndromic autism. The electron microscopy-based measurements of axonal diameter, axoplasm area and myelin thickness have characterized the abnormal velocity and capacity of axonal connections between hemispheres in subjects with autism and their contribution to autism clinical deficits.
The aim of the laboratory’s second project is to determine mechanisms of infiltration by macrophage/microglia of myeloid origin of the brains of people diagnosed with Down syndrome and mouse models leading to capillaries’ amyloidosis, fibrillar plaque formation, and neuronal degeneration and loss of function. A parallel ultrastructural study of human brain biopsy and transgenic mice brain with amyloidosis has the potential to identify treatment that will prevent brain amyloidosis, neuronal degeneration in the third decade, and dementia in the fourth decade of life of people with Down Syndrome.