Paul H. Patterson

Effects of intracellular expression of anti-huntingtin antibodies of various specificities on mutant huntingtin aggregation and toxicity.

Maternal infection: window on neuroimmune interactions in fetal brain development and mental illness.

Prenatal viral infection leads to pyramidal cell atrophy and macrocephaly in adulthood: implications for genesis of autism and schizophrenia.

Denervated Schwann cells attract macrophages by secretion of leukemia inhibitory factor (LIF) and monocyte chemoattractant protein-1 in a process regulated by interleukin-6 and LIF.

Maternal influenza infection causes marked behavioral and pharmacological changes in the offspring.

Developmental cooperation of leukemia inhibitory factor and insulin-like growth factor I in mice is tissue-specific and essential for lung maturation involving the transcription factors Sp3 and TTF-1.

Lymphocyte regulation of neuropeptide gene expression after neuronal injury.

Neonatal impact of leukemia inhibitory factor on neurobehavioral development in rats.

Antibodies against huntingtin: production and screening of monoclonals and single-chain recombinant forms.

Potent pro-inflammatory actions of leukemia inhibitory factor in the spinal cord of the adult mouse.

Activation of the IkappaB kinase complex and nuclear factor-kappaB contributes to mutant huntingtin neurotoxicity.

Targeted overexpression of leukemia inhibitory factor to preserve myocardium in a rat model of postinfarction heart failure.

Endothelin receptor B inhibition triggers apoptosis and enhances angiogenesis in melanomas.

Maternal influenza infection is likely to alter fetal brain development indirectly: the virus is not detected in the fetus.

Leukemia inhibitory factor promotes oligodendrocyte survival after spinal cord injury.

The cell cycle-apoptosis connection revisited in the adult brain.

Leukemia inhibitory factor is a key regulator of astrocytic, microglial and neuronal responses in a low-dose pilocarpine injury model.

Autism: neuropathology, alterations of the GABAergic system, and animal models.

Behavioral stress and tumor progression.

Leukemia inhibitory factor promotes neural stem cell self-renewal in the adult brain.

The neuropoietic cytokine family in development, plasticity, disease and injury.

A chronically implantable, hybrid cannula-electrode device for assessing the effects of molecules on electrophysiological signals in freely behaving animals.

Molecular basis for passive immunotherapy of Alzheimer's disease.

Maternal immune activation alters fetal brain development through interleukin-6.

Neuroscience. Maternal effects on schizophrenia risk.

Activation of the maternal immune system alters cerebellar development in the offspring.

Intrabodies binding the proline-rich domains of mutant huntingtin increase its turnover and reduce neurotoxicity.

Endothelin receptor B antagonists decrease glioma cell viability independently of their cognate receptor.

Immune involvement in schizophrenia and autism: etiology, pathology and animal models.

IKKalpha and IKKbeta regulation of DNA damage-induced cleavage of huntingtin.

Monoclonal antibodies recognize distinct conformational epitopes formed by polyglutamine in a mutant huntingtin fragment.

Cytokines and CNS development.

Intrabody gene therapy ameliorates motor, cognitive, and neuropathological symptoms in multiple mouse models of Huntington's disease.

IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome.

Maternal immune activation alters nonspatial information processing in the hippocampus of the adult offspring.

Pulsed UV light inactivation of Salmonella enteritidis on eggshells and its effects on egg quality.

Antibody therapy in neurodegenerative disease.

Maternal infection and schizophrenia: implications for prevention.

Activation of the maternal immune system induces endocrine changes in the placenta via IL-6.

Modeling autistic features in animals.

Perturbation with intrabodies reveals that calpain cleavage is required for degradation of huntingtin exon 1.

Maternal infection and immune involvement in autism.

Gene therapy in mouse models of huntington disease.

The role of IκB kinase complex in the neurobiology of Huntington's disease.

Maternal infection and autism.

Deletion of densin-180 results in abnormal behaviors associated with mental illness and reduces mGluR5 and DISC1 in the postsynaptic density fraction.

Maternal immune activation yields offspring displaying mouse versions of the three core symptoms of autism.

Exogenous leukemia inhibitory factor stimulates oligodendrocyte progenitor cell proliferation and enhances hippocampal remyelination.