Karen Duff

Imaging brain amyloid of Alzheimer disease in vivo in transgenic mice with an Abeta peptide radiopharmaceutical.

Statin therapy for Alzheimer's disease: will it work?

Cholesterol in Alzheimer's disease and tauopathy.

Novel therapeutic approach for the treatment of Alzheimer's disease by peripheral administration of agents with an affinity to beta-amyloid.

Organotypic slice cultures from transgenic mice as disease model systems.

Co-localization of cholesterol, apolipoprotein E and fibrillar Abeta in amyloid plaques.

Brain damage results in down-regulation of N-acetylaspartate as a neuronal osmolyte.

Use of in vivo models to study the role of cholesterol in the etiology of Alzheimer's disease.

Cdk5 is a key factor in tau aggregation and tangle formation in vivo.

Presenilin redistribution associated with aberrant cholesterol transport enhances beta-amyloid production in vivo.

Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms.

Detection of Alzheimer's amyloid in transgenic mice using magnetic resonance microimaging.

Evidence for peripheral clearance of cerebral Abeta protein following chronic, active Abeta immunization in PSAPP mice.

Changes in apolipoprotein E expression in response to dietary and pharmacological modulation of cholesterol.

Rapid neurofibrillary tangle formation after localized gene transfer of mutated tau.

MRI assessment of neuropathology in a transgenic mouse model of Alzheimer's disease.

Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration.

Transgenic mouse models of Alzheimer's disease: how useful have they been for therapeutic development?

Links between the pathology of Alzheimer's disease and vascular dementia.

Development of Abeta terminal end-specific antibodies and sensitive ELISA for Abeta variant.

Amyloid-beta deposition is associated with decreased hippocampal glucose metabolism and spatial memory impairment in APP/PS1 mice.

Rat transgenic models with a phenotype of intracellular Abeta accumulation in hippocampus and cortex.

Mostly separate distributions of CLAC- versus Abeta40- or thioflavin S-reactivities in senile plaques reveal two distinct subpopulations of beta-amyloid deposits.

Brain on steroids resists neurodegeneration.

Presenilin mutations in familial Alzheimer disease and transgenic mouse models accelerate neuronal lysosomal pathology.

Visualization of beta-amyloid plaques in a transgenic mouse model of Alzheimer's disease using MR microscopy without contrast reagents.

Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches.

Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo.

Histological co-localization of iron in Abeta plaques of PS/APP transgenic mice.

Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms.

An Abeta sequestration approach using non-antibody Abeta binding agents.

Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls.

Untangling memory deficits.

Macroautophagy--a novel Beta-amyloid peptide-generating pathway activated in Alzheimer's disease.

The amyloid pathology progresses in a neurotransmitter-specific manner.

Using proteomics and network analysis to elucidate the consequences of synaptic protein oxidation in a PS1 + AbetaPP mouse model of Alzheimer's disease.

The effects of ABCA1 on cholesterol efflux and Abeta levels in vitro and in vivo.

Cholesterol distribution, not total levels, correlate with altered amyloid precursor protein processing in statin-treated mice.

Normal and abnormal tau neurobiology.

Antibody against C-terminal Abeta selectively elevates plasma Abeta.

Anesthesia leads to tau hyperphosphorylation through inhibition of phosphatase activity by hypothermia.

Collapsin response mediator protein-2 hyperphosphorylation is an early event in Alzheimer's disease progression.

Increased dopaminergic neuron sensitivity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in transgenic mice expressing mutant A53T alpha-synuclein.

Insulin dysfunction induces in vivo tau hyperphosphorylation through distinct mechanisms.

Axonal transport rates in vivo are unaffected by tau deletion or overexpression in mice.

Interplay between cyclin-dependent kinase 5 and glycogen synthase kinase 3 beta mediated by neuregulin signaling leads to differential effects on tau phosphorylation and amyloid precursor protein processing.

Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processing.

Retromer deficiency observed in Alzheimer's disease causes hippocampal dysfunction, neurodegeneration, and Abeta accumulation.

Females exhibit more extensive amyloid, but not tau, pathology in an Alzheimer transgenic model.

A transgenic rat that develops Alzheimer's disease-like amyloid pathology, deficits in synaptic plasticity and cognitive impairment.

New directions for frontotemporal dementia drug discovery.

Is tau aggregation toxic or protective?

Anesthesia-induced hyperphosphorylation detaches 3-repeat tau from microtubules without affecting their stability in vivo.

Linking Abeta and tau in late-onset Alzheimer's disease: a dual pathway hypothesis.

Noninvasive and transient blood-brain barrier opening in the hippocampus of Alzheimer's double transgenic mice using focused ultrasound.

Optical visualization of Alzheimer's pathology via multiphoton-excited intrinsic fluorescence and second harmonic generation.

Acceleration and persistence of neurofibrillary pathology in a mouse model of tauopathy following anesthesia.

Structure-activity relationship of cyanine tau aggregation inhibitors.

Inhibition of tau polymerization with a cyanine dye in two distinct model systems.

Metabolic activity determines efficacy of macroautophagic clearance of pathological oligomeric alpha-synuclein.

Age-dependent impairment of cognitive and synaptic function in the htau mouse model of tau pathology.

Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria.

Lowering beta-amyloid levels rescues learning and memory in a Down syndrome mouse model.

Phenothiazine-mediated rescue of cognition in tau transgenic mice requires neuroprotection and reduced soluble tau burden.

Phospholipase d2 ablation ameliorates Alzheimer's disease-linked synaptic dysfunction and cognitive deficits.

Modulation of ABCA1 by an LXR agonist reduces β-amyloid levels and improves outcome after traumatic brain injury.

The phospholipase D1 pathway modulates macroautophagy.

Age and α-synuclein expression interact to reveal a dependence of dopaminergic axons on endogenous Akt/PKB signaling.

Microarray analysis of CA1 pyramidal neurons in a mouse model of tauopathy reveals progressive synaptic dysfunction.

Comparative lipidomic analysis of mouse and human brain with Alzheimer disease.

Trans-synaptic spread of tau pathology in vivo.