Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice

Research output: Contribution to journal › Journal article › Research › peer-review

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Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice. / Uribe, Valeria; Wong, Bibiana K Y; Graham, Rona K; Cusack, Corey L; Skotte, Niels H; Pouladi, Mahmoud A; Xie, Yuanyun; Feinberg, Konstantin; Ou, Yimiao; Ouyang, Yingbin; Deng, Yu; Franciosi, Sonia; Bissada, Nagat; Spreeuw, Amanda; Zhang, Weining; Ehrnhoefer, Dagmar E; Vaid, Kuljeet; Miller, Freda D; Deshmukh, Mohanish; Howland, David; Hayden, Michael R.

In: Human Molecular Genetics, Vol. 21, No. 9, 01.05.2012, p. 1954-67.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Uribe, V, Wong, BKY, Graham, RK, Cusack, CL, Skotte, NH, Pouladi, MA, Xie, Y, Feinberg, K, Ou, Y, Ouyang, Y, Deng, Y, Franciosi, S, Bissada, N, Spreeuw, A, Zhang, W, Ehrnhoefer, DE, Vaid, K, Miller, FD, Deshmukh, M, Howland, D & Hayden, MR 2012, 'Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice', Human Molecular Genetics, vol. 21, no. 9, pp. 1954-67. https://doi.org/10.1093/hmg/dds005

APA

Uribe, V., Wong, B. K. Y., Graham, R. K., Cusack, C. L., Skotte, N. H., Pouladi, M. A., Xie, Y., Feinberg, K., Ou, Y., Ouyang, Y., Deng, Y., Franciosi, S., Bissada, N., Spreeuw, A., Zhang, W., Ehrnhoefer, D. E., Vaid, K., Miller, F. D., Deshmukh, M., ... Hayden, M. R. (2012). Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice. Human Molecular Genetics, 21(9), 1954-67. https://doi.org/10.1093/hmg/dds005

Vancouver

Uribe V, Wong BKY, Graham RK, Cusack CL, Skotte NH, Pouladi MA et al. Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice. Human Molecular Genetics. 2012 May 1;21(9):1954-67. https://doi.org/10.1093/hmg/dds005

Author

Uribe, Valeria ; Wong, Bibiana K Y ; Graham, Rona K ; Cusack, Corey L ; Skotte, Niels H ; Pouladi, Mahmoud A ; Xie, Yuanyun ; Feinberg, Konstantin ; Ou, Yimiao ; Ouyang, Yingbin ; Deng, Yu ; Franciosi, Sonia ; Bissada, Nagat ; Spreeuw, Amanda ; Zhang, Weining ; Ehrnhoefer, Dagmar E ; Vaid, Kuljeet ; Miller, Freda D ; Deshmukh, Mohanish ; Howland, David ; Hayden, Michael R. / Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice. In: Human Molecular Genetics. 2012 ; Vol. 21, No. 9. pp. 1954-67.

Bibtex

@article{eea7df7eb54946ae90ab41e83e5b0cf6,
title = "Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice",
abstract = "Apoptosis, or programmed cell death, is a cellular pathway involved in normal cell turnover, developmental tissue remodeling, embryonic development, cellular homeostasis maintenance and chemical-induced cell death. Caspases are a family of intracellular proteases that play a key role in apoptosis. Aberrant activation of caspases has been implicated in human diseases. In particular, numerous findings implicate Caspase-6 (Casp6) in neurodegenerative diseases, including Alzheimer disease (AD) and Huntington disease (HD), highlighting the need for a deeper understanding of Casp6 biology and its role in brain development. The use of targeted caspase-deficient mice has been instrumental for studying the involvement of caspases in apoptosis. The goal of this study was to perform an in-depth neuroanatomical and behavioral characterization of constitutive Casp6-deficient (Casp6-/-) mice in order to understand the physiological function of Casp6 in brain development, structure and function. We demonstrate that Casp6-/- neurons are protected against excitotoxicity, nerve growth factor deprivation and myelin-induced axonal degeneration. Furthermore, Casp6-deficient mice show an age-dependent increase in cortical and striatal volume. In addition, these mice show a hypoactive phenotype and display learning deficits. The age-dependent behavioral and region-specific neuroanatomical changes observed in the Casp6-/- mice suggest that Casp6 deficiency has a more pronounced effect in brain regions that are involved in neurodegenerative diseases, such as the striatum in HD and the cortex in AD.",
keywords = "Aging, Alzheimer Disease, Animals, Apoptosis, Base Sequence, Behavior, Animal, Brain, Caspase 6, Humans, Huntington Disease, Mice, Mice, Knockout, Motor Activity, Nerve Degeneration, Neurons, RNA, Messenger, Receptors, N-Methyl-D-Aspartate",
author = "Valeria Uribe and Wong, {Bibiana K Y} and Graham, {Rona K} and Cusack, {Corey L} and Skotte, {Niels H} and Pouladi, {Mahmoud A} and Yuanyun Xie and Konstantin Feinberg and Yimiao Ou and Yingbin Ouyang and Yu Deng and Sonia Franciosi and Nagat Bissada and Amanda Spreeuw and Weining Zhang and Ehrnhoefer, {Dagmar E} and Kuljeet Vaid and Miller, {Freda D} and Mohanish Deshmukh and David Howland and Hayden, {Michael R}",
year = "2012",
month = may,
day = "1",
doi = "10.1093/hmg/dds005",
language = "English",
volume = "21",
pages = "1954--67",
journal = "Human Molecular Genetics",
issn = "0964-6906",
publisher = "Oxford University Press",
number = "9",

}

RIS

TY - JOUR

T1 - Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice

AU - Uribe, Valeria

AU - Wong, Bibiana K Y

AU - Graham, Rona K

AU - Cusack, Corey L

AU - Skotte, Niels H

AU - Pouladi, Mahmoud A

AU - Xie, Yuanyun

AU - Feinberg, Konstantin

AU - Ou, Yimiao

AU - Ouyang, Yingbin

AU - Deng, Yu

AU - Franciosi, Sonia

AU - Bissada, Nagat

AU - Spreeuw, Amanda

AU - Zhang, Weining

AU - Ehrnhoefer, Dagmar E

AU - Vaid, Kuljeet

AU - Miller, Freda D

AU - Deshmukh, Mohanish

AU - Howland, David

AU - Hayden, Michael R

PY - 2012/5/1

Y1 - 2012/5/1

N2 - Apoptosis, or programmed cell death, is a cellular pathway involved in normal cell turnover, developmental tissue remodeling, embryonic development, cellular homeostasis maintenance and chemical-induced cell death. Caspases are a family of intracellular proteases that play a key role in apoptosis. Aberrant activation of caspases has been implicated in human diseases. In particular, numerous findings implicate Caspase-6 (Casp6) in neurodegenerative diseases, including Alzheimer disease (AD) and Huntington disease (HD), highlighting the need for a deeper understanding of Casp6 biology and its role in brain development. The use of targeted caspase-deficient mice has been instrumental for studying the involvement of caspases in apoptosis. The goal of this study was to perform an in-depth neuroanatomical and behavioral characterization of constitutive Casp6-deficient (Casp6-/-) mice in order to understand the physiological function of Casp6 in brain development, structure and function. We demonstrate that Casp6-/- neurons are protected against excitotoxicity, nerve growth factor deprivation and myelin-induced axonal degeneration. Furthermore, Casp6-deficient mice show an age-dependent increase in cortical and striatal volume. In addition, these mice show a hypoactive phenotype and display learning deficits. The age-dependent behavioral and region-specific neuroanatomical changes observed in the Casp6-/- mice suggest that Casp6 deficiency has a more pronounced effect in brain regions that are involved in neurodegenerative diseases, such as the striatum in HD and the cortex in AD.

AB - Apoptosis, or programmed cell death, is a cellular pathway involved in normal cell turnover, developmental tissue remodeling, embryonic development, cellular homeostasis maintenance and chemical-induced cell death. Caspases are a family of intracellular proteases that play a key role in apoptosis. Aberrant activation of caspases has been implicated in human diseases. In particular, numerous findings implicate Caspase-6 (Casp6) in neurodegenerative diseases, including Alzheimer disease (AD) and Huntington disease (HD), highlighting the need for a deeper understanding of Casp6 biology and its role in brain development. The use of targeted caspase-deficient mice has been instrumental for studying the involvement of caspases in apoptosis. The goal of this study was to perform an in-depth neuroanatomical and behavioral characterization of constitutive Casp6-deficient (Casp6-/-) mice in order to understand the physiological function of Casp6 in brain development, structure and function. We demonstrate that Casp6-/- neurons are protected against excitotoxicity, nerve growth factor deprivation and myelin-induced axonal degeneration. Furthermore, Casp6-deficient mice show an age-dependent increase in cortical and striatal volume. In addition, these mice show a hypoactive phenotype and display learning deficits. The age-dependent behavioral and region-specific neuroanatomical changes observed in the Casp6-/- mice suggest that Casp6 deficiency has a more pronounced effect in brain regions that are involved in neurodegenerative diseases, such as the striatum in HD and the cortex in AD.

KW - Aging

KW - Alzheimer Disease

KW - Animals

KW - Apoptosis

KW - Base Sequence

KW - Behavior, Animal

KW - Brain

KW - Caspase 6

KW - Humans

KW - Huntington Disease

KW - Mice

KW - Mice, Knockout

KW - Motor Activity

KW - Nerve Degeneration

KW - Neurons

KW - RNA, Messenger

KW - Receptors, N-Methyl-D-Aspartate

U2 - 10.1093/hmg/dds005

DO - 10.1093/hmg/dds005

M3 - Journal article

C2 - 22262731

VL - 21

SP - 1954

EP - 1967

JO - Human Molecular Genetics

JF - Human Molecular Genetics

SN - 0964-6906

IS - 9

ER -

ID: 153451495