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  • The background is an image of neurons (blue). Some of them express the new amyloid precursor protein reporter (green) and a synapse-marker, Synaptophysin-pHTomato (red). The rendering at the lower left corner illustrates the Alzheimer’s disease etiology model derived from the study, in which a variety of pathological contributors like aging and Abeta converge on presynaptic cholesterol and the disruption of cholesterol homeostasis diverges to various pathological outcomes like synaptic dysfunction and neuronal loss.
    Qi Zhang, Ph.D. and Claire E. DelBove
    The background is an image of neurons (blue). Some of them express the new amyloid precursor protein reporter (green) and a synapse-marker, Synaptophysin-pHTomato (red). The rendering at the lower left corner illustrates the Alzheimer’s disease etiology model derived from the study, in which a variety of pathological contributors like aging and Abeta converge on presynaptic cholesterol and the disruption of cholesterol homeostasis diverges to various pathological outcomes like synaptic dysfunction and neuronal loss.
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