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2 results on '"Zoe Murphy"'

1. Testicular degeneration in Huntington disease

Author

Jeremy M. Van Raamsdonk, Zoe Murphy, David M. Selva, Reza Hamidizadeh, Jacqueline Pearson, Ǻsa Petersén, Maria Björkqvist, Cameron Muir, Ian R. Mackenzie, Geoffrey L. Hammond, A. Wayne Vogl, Michael R. Hayden, and Blair R. Leavitt

Subjects
Huntington disease, Huntingtin, Testis, Hypothalamic–pituitary–gonadal axis, Testosterone, YAC128 mouse model, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Huntington disease (HD) is an adult onset, neurodegenerative disorder that results from CAG expansion in the HD gene. Recent work has demonstrated testicular degeneration in mouse models of HD and alterations in the hypothalamic–pituitary–gonadal (HPG) axis in HD patients. Here, we show that HD patients have specific testicular pathology with reduced numbers of germ cells and abnormal seminiferous tubule morphology. In the YAC128 mouse model, testicular degeneration develops prior to 12 months of age, but at 12 months, there is no evidence for decreased testosterone levels or loss of GnRH neurons in the hypothalamus. This suggests that testicular pathology results from a direct toxic effect of mutant huntingtin in the testis and is supported by the fact that huntingtin is highly expressed in the affected cell populations in the testis. Understanding the pathogenesis of HD in the testis may reveal common critical pathways which lead to degeneration in both the brain and testis.

Published
2007
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2. Testicular degeneration in Huntington disease

Author

A. Wayne Vogl, Jeremy M. Van Raamsdonk, Maria Björkqvist, Cameron Muir, Blair R. Leavitt, David M. Selva, Reza Hamidizadeh, Zoe Murphy, Geoffrey L. Hammond, Michael R. Hayden, Åsa Petersén, Jacqueline Pearson, and Ian R. A. Mackenzie

Subjects
Adult, Male, medicine.medical_specialty, Hypothalamo-Hypophyseal System, endocrine system, Huntingtin, Hypothalamic–pituitary–gonadal axis, Mice, Transgenic, Nerve Tissue Proteins, YAC128 mouse model, Degeneration (medical), Biology, Testicular Diseases, lcsh:RC321-571, Pathogenesis, Gonadotropin-Releasing Hormone, Mice, Internal medicine, Testis, Huntingtin Protein, medicine, Animals, Humans, Testosterone, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Aged, Neurons, Nuclear Proteins, Middle Aged, Seminiferous Tubules, Huntington disease, Disease Models, Animal, Seminiferous tubule, medicine.anatomical_structure, Endocrinology, Germ Cells, Neurology, Hypothalamus
Abstract

Huntington disease (HD) is an adult onset, neurodegenerative disorder that results from CAG expansion in the HD gene. Recent work has demonstrated testicular degeneration in mouse models of HD and alterations in the hypothalamic-pituitary-gonadal (HPG) axis in HD patients. Here, we show that HD patients have specific testicular pathology with reduced numbers of germ cells and abnormal seminiferous tubule morphology. In the YAC128 mouse model, testicular degeneration develops prior to 12 months of age, but at 12 months, there is no evidence for decreased testosterone levels or loss of GnRH neurons in the hypothalamus. This suggests that testicular pathology results from a direct toxic effect of mutant huntingtin in the testis and is supported by the fact that huntingtin is highly expressed in the affected cell populations in the testis. Understanding the pathogenesis of HD in the testis may reveal common critical pathways which lead to degeneration in both the brain and testis.

Published
2007

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