Kilbridge, Joshua

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

Holtzman, D. M., Santucci, D., Kilbridge, J., Chua-Couzens, J., Fontana, D. J., Daniels, S. E., Johnson, R. M., Chen, K., Sun, Y., Carlson, E., et al. (1996) · Proceedings of the National Academy of Sciences

Down syndrome and intellectual disability researchAlzheimer's disease research and treatments

Cited by 448

Ts1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities

Sago, H., Carlson, E. J., Smith, D. J., Kilbridge, J., Rubin, E. M., Mobley, W. C., Epstein, C. J., & Huang, T.-T. (1998) · Proceedings of the National Academy of Sciences

Down syndrome and intellectual disability researchGenetics and Neurodevelopmental Disorders

Cited by 382

Low density lipoprotein receptor-related protein mediates apolipoprotein E-dependent neurite outgrowth in a central nervous system-derived neuronal cell line.

Holtzman, D. M., Pitas, R. E., Kilbridge, J., Nathan, B., Mahley, R. W., Bu, G., & Schwartz, A. L. (1995) · Proceedings of the National Academy of Sciences

Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Cited by 349

Failed retrograde transport of NGF in a mouse model of Down's syndrome: Reversal of cholinergic neurodegenerative phenotypes following NGF infusion

Cooper, J. D., Salehi, A., Delcroix, J.-D., Howe, C. L., Belichenko, P. V., Chua-Couzens, J., Kilbridge, J. F., Carlson, E. J., Epstein, C. J., & Mobley, W. C. (2001) · Proceedings of the National Academy of Sciences

Alzheimer's disease research and treatmentsDown syndrome and intellectual disability research

Cited by 336

Evidence for normal aging of the septo-hippocampal cholinergic system in apoE (−/−) mice but impaired clearance of axonal degeneration products following injury

Fagan, A. M., Murphy, B. A., Patel, S. N., Kilbridge, J. F., Mobley, W. C., Bu, G., & Holtzman, D. M. (1998) · Experimental Neurology

Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Cited by 116