William C. Mobley

Traffic at the intersection of neurotrophic factor signaling and neurodegeneration.

NGF signaling in sensory neurons: evidence that early endosomes carry NGF retrograde signals.

Trafficking the NGF signal: implications for normal and degenerating neurons.

Signaling endosome hypothesis: A cellular mechanism for long distance communication.

Going the distance, or not, with neurotrophin signals.

Hippocampal long-term potentiation suppressed by increased inhibition in the Ts65Dn mouse, a genetic model of Down syndrome.

Late onset neurodegeneration in the Cln3-/- mouse model of juvenile neuronal ceroid lipofuscinosis is preceded by low level glial activation.

An AUPN/ANA survey of department leader opinions on the health of US academic neurology.

Synaptic structural abnormalities in the Ts65Dn mouse model of Down Syndrome.

Long-distance retrograde neurotrophic signaling.

Identification and characterization of a new Down syndrome model, Ts[Rb(12.1716)]2Cje, resulting from a spontaneous Robertsonian fusion between T(171)65Dn and mouse chromosome 12.

TrkB binds and tyrosine-phosphorylates Tiam1, leading to activation of Rac1 and induction of changes in cellular morphology.

Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.

Retrolinkin, a membrane protein, plays an important role in retrograde axonal transport.

Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationships.

One at a time, live tracking of NGF axonal transport using quantum dots.

A functional dynein-microtubule network is required for NGF signaling through the Rap1/MAPK pathway.

Using mouse models to explore genotype-phenotype relationship in Down syndrome.

Membrane targeting by APPL1 and APPL2: dynamic scaffolds that oligomerize and bind phosphoinositides.

Sleep and EEG features in genetic models of Down syndrome.

Comparative study of brain morphology in Mecp2 mutant mouse models of Rett syndrome.

Review of the toxicology of chlorpyrifos with an emphasis on human exposure and neurodevelopment.

Endophilin B1 as a novel regulator of nerve growth factor/ TrkA trafficking and neurite outgrowth.

The coming of age of axonal neurotrophin signaling endosomes.

Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of Down syndrome.

Evidence for both neuronal cell autonomous and nonautonomous effects of methyl-CpG-binding protein 2 in the cerebral cortex of female mice with Mecp2 mutation.

Widespread changes in dendritic and axonal morphology in Mecp2-mutant mouse models of Rett syndrome: evidence for disruption of neuronal networks.

The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome.

The 50th anniversary of the discovery of trisomy 21: the past, present, and future of research and treatment of Down syndrome.

Deficiencies in the region syntenic to human 21q22.3 cause cognitive deficits in mice.

Modulation of gamma-secretase reduces beta-amyloid deposition in a transgenic mouse model of Alzheimer's disease.

Effects of individual segmental trisomies of human chromosome 21 syntenic regions on hippocampal long-term potentiation and cognitive behaviors in mice.

Implications for treatment: GABAA receptors in aging, Down syndrome and Alzheimer's disease.

Comprehensive behavioral phenotyping of Ts65Dn mouse model of Down syndrome: activation of β1-adrenergic receptor by xamoterol as a potential cognitive enhancer.

Enantioselective synthesis of (-)-jiadifenin, a potent neurotrophic modulator.

Mouse models for Down syndrome-associated developmental cognitive disabilities.

Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome.

Genetic analysis of Down syndrome facilitated by mouse chromosome engineering.

Cognitive and pharmacological insights from the Ts65Dn mouse model of Down syndrome.

Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.

Potential use of γ-secretase modulators in the treatment of Alzheimer disease.

Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome.

Illicium sesquiterpenes: divergent synthetic strategy and neurotrophic activity studies.

Aging and intellectual disability: Insights from mouse models of down syndrome.

Human chromosome 21 orthologous region on mouse chromosome 17 is a major determinant of Down syndrome-related developmental cognitive deficits.

The challenge of connecting the dots in the B.R.a.I.N.

Soluble γ-Secretase Modulators Selectively Inhibit the Production of the 42-Amino Acid Amyloid β Peptide Variant and Augment the Production of Multiple Carboxy-Truncated Amyloid β Species.