David R Borchelt

Environmental Enrichment Exacerbates Amyloid Plaque Formation in a Transgenic Mouse Model of Alzheimer Disease

D. Borchelt, V. Gonzales, J. Jankowsky, 2003, Journal of neuropathology and experimental neurology.

N-Terminal Proteolysis of Full-Length Mutant Huntingtin in an Inducible PC12 Cell Model of Huntington’s Disease

Christopher A Ross, D. Borchelt, M. Hayden, 2007, Cell cycle.

Persistent Amyloidosis following Suppression of Aβ Production in a Transgenic Model of Alzheimer Disease

H. Lester, D. Borchelt, A. Savonenko, 2005, PLoS medicine.

An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria

D. Borchelt, D. Price, P. Wong, 1995, Neuron.

Transgenic mouse models of neurodegenerative disease: Opportunities for therapeutic development

Alena Savonenko, D. Borchelt, A. Savonenko, 2002, Current neurology and neuroscience reports.

Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase.

D. Borchelt, S. Younkin, L. Younkin, 2004, Human molecular genetics.

Quantitative Comparison of Dense-Core Amyloid Plaque Accumulation in Amyloid-β Protein Precursor Transgenic Mice.

Peng Liu, K. Zahs, D. Borchelt, 2017, Journal of Alzheimer's disease : JAD.