V. Gonzales

发表

Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins

D. Borchelt, D. Price, N. Jenkins, 1997, Neuron.

Environmental Enrichment Mitigates Cognitive Deficits in a Mouse Model of Alzheimer's Disease

D. Borchelt, A. Savonenko, S. Younkin, 2005, The Journal of Neuroscience.

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

Joanna L. Jankowsky, Nancy A. Jenkins, D. Borchelt, 2004 .

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.

Abeta deposition does not cause the aggregation of endogenous tau in transgenic mice.

D. Borchelt, V. Gonzales, Guilian M. Xu, 2002, Alzheimer disease and associated disorders.

Differential regulation of small heat shock proteins in transgenic mouse models of neurodegenerative diseases

D. Borchelt, Michael K. Lee, V. Gonzales, 2008, Neurobiology of Aging.

High rate of hypomorphic variants as the cause of inherited ataxia and related diseases: study of a cohort of 366 families

V. Fraix, L. Kremer, M. Koenig, 2021, Genetics in Medicine.

A Deposition Does Not Cause the Aggregation of Endogenous Tau in Transgenic Mice

D. Borchelt, V. Gonzales, Guilian M. Xu, 2002 .

Coincident thresholds of mutant protein for paralytic disease and protein aggregation caused by restrictively expressed superoxide dismutase cDNA

D. Borchelt, N. Jenkins, V. Gonzales, 2005, Neurobiology of Disease.

Accumulation of proteolytic fragments of mutant presenilin 1 and accelerated amyloid deposition are co-regulated in transgenic mice

D. Borchelt, N. Jenkins, S. Sisodia, 2002, Neurobiology of Aging.

APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1

D. Borchelt, N. Jenkins, V. Gonzales, 2004, Neurobiology of Aging.

Open access, freely available online PLoS MEDICINE Persistent Amyloidosis following Suppression of Ab Production in a Transgenic Model of Alzheimer Disease

H. Lester, D. Borchelt, A. Savonenko, 2022 .

Copper-binding-site-null SOD1 causes ALS in transgenic mice: aggregates of non-native SOD1 delineate a common feature.

D. Borchelt, N. Jenkins, V. Gonzales, 2003, Human molecular genetics.

Fibrillar Inclusions and Motor Neuron Degeneration in Transgenic Mice Expressing Superoxide Dismutase 1 with a Disrupted Copper-Binding Site

D. Borchelt, N. Jenkins, V. Gonzales, 2002, Neurobiology of Disease.

Distinct Behavioral and Neuropathological Abnormalities in Transgenic Mouse Models of HD and DRPLA

D. Borchelt, D. Price, C. Ross, 2001, Neurobiology of Disease.

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.

Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice

D. Borchelt, Nianwei Lin, Ning Li, 2008, PloS one.

Characterization of Huntingtin Pathologic Fragments in Human Huntington Disease, Transgenic Mice, and Cell Models

D. Borchelt, C. Ross, Andrew T. N. Tebbenkamp, 2007, Journal of neuropathology and experimental neurology.

Nuclear-targeting of mutant huntingtin fragments produces Huntington's disease-like phenotypes in transgenic mice.

D. Borchelt, A. Savonenko, C. Ross, 2004, Human molecular genetics.

Nuclear Accumulation of Truncated Atrophin-1 Fragments in a Transgenic Mouse Model of DRPLA

D. Borchelt, D. Price, C. Ross, 1999, Neuron.

Episodic-like memory deficits in the APPswe/PS1dE9 mouse model of Alzheimer's disease: Relationships to β-amyloid deposition and neurotransmitter abnormalities

D. Borchelt, A. Savonenko, V. Gonzales, 2005, Neurobiology of Disease.

Somatodendritic accumulation of misfolded SOD1-L126Z in motor neurons mediates degeneration: alphaB-crystallin modulates aggregation.

D. Borchelt, N. Jenkins, Hong Li, 2005, Human molecular genetics.

Rodent Aβ Modulates the Solubility and Distribution of Amyloid Deposits in Transgenic Mice*

H. Lester, D. Borchelt, S. Younkin, 2007, Journal of Biological Chemistry.

Rapid detection of protein aggregates in the brains of Alzheimer patients and transgenic mouse models of amyloidosis.

D. Borchelt, V. Gonzales, Guilian Xu, 2002, Alzheimer disease and associated disorders.