Ju Gao

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Journals/Publications

• Gao, J., Leinonen, H., Wang, E. J., Ding, M., Perry, G., Palczewski, K., & Wang, X. (2024). Sex-Specific Early Retinal Dysfunction in Mutant TDP-43 Transgenic Mice. Journal of Alzheimer's disease : JAD, 97(2), 927-937.
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  Increasing evidence has highlighted retinal impairments in neurodegenerative diseases. Dominant mutations in TAR DNA-binding protein 43 (TDP-43) cause amyotrophic lateral sclerosis (ALS), and the accumulation of TDP-43 in the cytoplasm is a pathological hallmark of ALS, frontotemporal dementia (FTD), and many other neurodegenerative diseases.
• Gao, J., Okolo, O., Siedlak, S. L., Friedland, R. P., & Wang, X. (2024). Ferritin is closely associated with microglia in amyotrophic lateral sclerosis. Journal of neuropathology and experimental neurology, 83(11), 917-926.
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  Iron deposition is a hallmark of amyotrophic lateral sclerosis (ALS) and has been strongly implicated in its pathogenesis. As a byproduct of cellular oxidative stress, iron dysregulation modifies basal levels of the regulatory iron-binding protein ferritin. Examination of thoracic and lumbar spinal cord tissues found increased ferritin immunostaining in white matter axons that corresponded to areas of increased microgliosis in 8 ALS patients versus 8 normal subjects. Gray matter areas containing the motor neurons also demonstrated increased ferritin and microglia in ALS compared to controls but at lower levels than in the white matter. Motor neurons with or without TDP-43 inclusions did not demonstrate either increased ferritin or associated microglial activation. We also observed an association of ferritin with microglia in cerebral cortical tissue samples of ALS cases and in the spinal cord tissues of transgenic mice expressing the SOD1G93A mutation. Elevated ferritin levels were detected in the insoluble fraction from spinal cord tissues of individuals with ALS. These findings suggest that activated microglia and increased ferritin may play significant roles in ALS progression since they are found closely associated in areas of axonal and cortical degeneration.
• Xiyang, Y., Gao, J., Ding, M., Ren, X., Appleby, B. S., Leverenz, J. B., Miyagi, M., Pillai, J. A., Perry, G., & Wang, X. (2024). Exacerbated mitochondrial dynamic abnormalities without evident tau pathology in rapidly progressive Alzheimer's disease. Journal of Alzheimer's disease : JAD, 102(4), 1074-1083.
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  Rapidly progressive Alzheimer's disease (rpAD) is a clinical subtype distinguished by its rapid cognitive decline and shorter disease duration. rpAD, like typical AD (tAD), is characterized by underlying neuropathology of amyloid plaques and neurofibrillary tangles. There is early evidence that the composition of amyloid plaques could vary between the rpAD and tAD. Differences in tau pathology between rpAD and tAD are also of interest. Additionally, mitochondrial dysfunction is a key early-stage change in tAD but has not yet been evaluated in rpAD.