Joanna L. Jankowsky

Transgenic mouse models of neurodegenerative disease: opportunities for therapeutic development.

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

Environmental enrichment exacerbates amyloid plaque formation in a transgenic mouse model of Alzheimer disease.

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

Environmental enrichment mitigates cognitive deficits in a mouse model of Alzheimer's disease.

Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease.

Rodent A beta modulates the solubility and distribution of amyloid deposits in transgenic mice.

Alzheimer's-type amyloidosis in transgenic mice impairs survival of newborn neurons derived from adult hippocampal neurogenesis.

GABA transporter function, oligomerization state, and anchoring: correlates with subcellularly resolved FRET.

Remote sites of structural atrophy predict later amyloid formation in a mouse model of Alzheimer's disease.

Robust amyloid clearance in a mouse model of Alzheimer's disease provides novel insights into the mechanism of amyloid-beta immunotherapy.

Neuronal aggregates are associated with phenotypic onset in the R6/2 Huntington's disease transgenic mouse.

Transgenic APP expression during postnatal development causes persistent locomotor hyperactivity in the adult.

Strain background influences neurotoxicity and behavioral abnormalities in mice expressing the tetracycline transactivator.

Viral transduction of the neonatal brain delivers controllable genetic mosaicism for visualising and manipulating neuronal circuits in vivo.

Capsid serotype and timing of injection determines AAV transduction in the neonatal mice brain.

Wild-type neural progenitors divide and differentiate normally in an amyloid-rich environment.

Specificity and efficiency of reporter expression in adult neural progenitors vary substantially among nestin-CreER(T2) lines.

Genetic suppression of transgenic APP rescues Hypersynchronous network activity in a mouse model of Alzeimer's disease.

Impairments in experience-dependent scaling and stability of hippocampal place fields limit spatial learning in a mouse model of Alzheimer's disease.

Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease.

Cerebral vascular leak in a mouse model of amyloid neuropathology.