Carol M. Troy

Nedd2 is required for apoptosis after trophic factor withdrawal, but not superoxide dismutase (SOD1) downregulation, in sympathetic neurons and PC12 cells.

Multiple pathways of neuronal death induced by DNA-damaging agents, NGF deprivation, and oxidative stress.

Caspase-2 (Nedd-2) processing and death of trophic factor-deprived PC12 cells and sympathetic neurons occur independently of caspase-3 (CPP32)-like activity.

Caspase-2 mediates neuronal cell death induced by beta-amyloid.

Death in the balance: alternative participation of the caspase-2 and -9 pathways in neuronal death induced by nerve growth factor deprivation.

Mechanisms of p75-mediated death of hippocampal neurons. Role of caspases.

Caspases on the brain.

Divergence of the apoptotic pathways induced by 4-hydroxynonenal and amyloid beta-protein.

Balancing neuronal death.

Highly efficient small interfering RNA delivery to primary mammalian neurons induces MicroRNA-like effects before mRNA degradation.

Caspase function in neuronal death: delineation of the role of caspases in ischemia.

Cell cycle molecules define a pathway required for neuron death in development and disease.

Bim is elevated in Alzheimer's disease neurons and is required for beta-amyloid-induced neuronal apoptosis.

Mechanisms of neuronal death in disease: defining the models and the players.

Caspase-2: vestigial remnant or master regulator?

The Parkinson disease protein leucine-rich repeat kinase 2 transduces death signals via Fas-associated protein with death domain and caspase-8 in a cellular model of neurodegeneration.

Selective inhibition of hypoxia-inducible factor (HIF) prolyl-hydroxylase 1 mediates neuroprotection against normoxic oxidative death via HIF- and CREB-independent pathways.

Cystatin C protects neuronal cells from amyloid-beta-induced toxicity.

Regulation of caspases in the nervous system implications for functions in health and disease.

Endogenous amyloid-β is necessary for hippocampal synaptic plasticity and memory.

Intranasal delivery of caspase-9 inhibitor reduces caspase-6-dependent axon/neuron loss and improves neurological function after stroke.

Neuronal caspase 2 activity and function requires RAIDD, but not PIDD.

Caspase inhibitors: prospective therapies for stroke.

Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection.

Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice.

Caspase-2 is essential for c-Jun transcriptional activation and Bim induction in neuron death.

Combined suppression of CASP2 and CASP6 protects retinal ganglion cells from apoptosis and promotes axon regeneration through CNTF-mediated JAK/STAT signalling.

Axonally synthesized ATF4 transmits a neurodegenerative signal across brain regions.

Caspase-9 mediates photoreceptor death after blunt ocular trauma.

Caspases: therapeutic targets in neurologic disease.

Mutations in CRADD Result in Reduced Caspase-2-Mediated Neuronal Apoptosis and Cause Megalencephaly with a Rare Lissencephaly Variant.

Caspase-2 and tau-a toxic partnership?

Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice.

Endothelial activation of caspase-9 promotes neurovascular injury in retinal vein occlusion.

Author Correction: Endothelial activation of caspase-9 promotes neurovascular injury in retinal vein occlusion.

Caspase-9: A Multimodal Therapeutic Target With Diverse Cellular Expression in Human Disease.