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Early Increase in Extrasynaptic NMDA Receptor Signaling and Expression Contributes to Phenotype Onset in Huntington's Disease Mice

Neuron (Cambridge, Mass.), 2010-01, Vol.65 (2), p.178-190

2010

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Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingtin

Nature medicine, 2009-12, Vol.15 (12), p.1407-1413

2009

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Cleavage at the Caspase-6 Site Is Required for Neuronal Dysfunction and Degeneration Due to Mutant Huntingtin

Cell, 2006-06, Vol.125 (6), p.1179-1191

2006

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Characterization of age-associated changes in peripheral organ and brain region weights in C57BL/6 mice

Experimental gerontology, 2015-03, Vol.63, p.27-34

2015

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Activation of caspase‐6 and cleavage of caspase‐6 substrates is an early event in NMDA receptor–mediated excitotoxicity

Journal of neuroscience research, 2018-03, Vol.96 (3), p.391-406

2018

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Volumetric MRI Demonstrates Atrophy of the Olfactory Cortex in AD

Current Alzheimer research, 2020-01, Vol.17 (10), p.904-915

2020

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Partial rescue of some features of Huntington Disease in the genetic absence of caspase-6 in YAC128 mice

Neurobiology of disease, 2015-04, Vol.76, p.24-36

2015

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Absence of Behavioral Abnormalities and Neurodegeneration in vivo despite Widespread Neuronal Huntingtin Inclusions

Proceedings of the National Academy of Sciences - PNAS, 2005-08, Vol.102 (32), p.11402-11407

2005

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Full length mutant huntingtin is required for altered Ca2+ signaling and apoptosis of striatal neurons in the YAC mouse model of Huntington's disease

Neurobiology of disease, 2008-07, Vol.31 (1), p.80-88

2008

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Accumulation of N-terminal mutant huntingtin in mouse and monkey models implicated as a pathogenic mechanism in Huntington's disease

Human molecular genetics, 2008-09, Vol.17 (17), p.2738-2751

2008

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

Human molecular genetics, 2012-05, Vol.21 (9), p.1954-1967

2012

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Transgenic mouse model expressing the caspase 6 fragment of mutant huntingtin

The Journal of neuroscience, 2012-01, Vol.32 (1), p.183-193

2012

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Phosphorylation of huntingtin reduces the accumulation of its nuclear fragments

Molecular and cellular neuroscience, 2009-02, Vol.40 (2), p.121-127

2009

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NP03, a novel low-dose lithium formulation, is neuroprotective in the YAC128 mouse model of Huntington disease

Neurobiology of disease, 2012-12, Vol.48 (3), p.282-289

2012

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Elevated brain 3-hydroxykynurenine and quinolinate levels in Huntington disease mice

Neurobiology of disease, 2006-07, Vol.23 (1), p.190-197

2006

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Wild‐type huntingtin protects neurons from excitotoxicity

Journal of neurochemistry, 2006-02, Vol.96 (4), p.1121-1129

2006

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Caspase Cleavage of Mutant Huntingtin Precedes Neurodegeneration in Huntington's Disease

The Journal of neuroscience, 2002-09, Vol.22 (18), p.7862-7872

2002

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Phenotypic abnormalities in the YAC128 mouse model of Huntington disease are penetrant on multiple genetic backgrounds and modulated by strain

Neurobiology of disease, 2007-04, Vol.26 (1), p.189-200

2007

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Polyglutamine-Modulated Striatal Calpain Activity in YAC Transgenic Huntington Disease Mouse Model: Impact on NMDA Receptor Function and Toxicity

The Journal of neuroscience, 2008-11, Vol.28 (48), p.12725-12735

2008

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Specific olfactory deficit patterns observed in seniors and associated with cognitive decline

Progress in neuro-psychopharmacology & biological psychiatry, 2023-08, Vol.126, p.110775-110775, Article 110775

2023

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Caspase-6 and neurodegeneration

Trends in neurosciences (Regular ed.), 2011-12, Vol.34 (12), p.646-656

2011

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Olfactory Dysfunction Associated with Cognitive Decline in an Elderly Population

Experimental aging research, 2024-01, Vol.50 (1), p.1-16

2024

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Striatal neuronal apoptosis is preferentially enhanced by NMDA receptor activation in YAC transgenic mouse model of Huntington disease

Neurobiology of disease, 2006-02, Vol.21 (2), p.392-403

2006

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Amelioration of Cognitive and Olfactory System Deficits in APOE4 Transgenic Mice with DHA Treatment

Molecular neurobiology, 2023-10, Vol.60 (10), p.5624-5641

2023

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Early Increase in Extrasynaptic NMDA Receptor Signaling and Expression Contributes to Phenotype Onset in Huntington's Disease Mice

Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingtin

Cleavage at the Caspase-6 Site Is Required for Neuronal Dysfunction and Degeneration Due to Mutant Huntingtin

Characterization of age-associated changes in peripheral organ and brain region weights in C57BL/6 mice

Activation of caspase‐6 and cleavage of caspase‐6 substrates is an early event in NMDA receptor–mediated excitotoxicity

Volumetric MRI Demonstrates Atrophy of the Olfactory Cortex in AD

Partial rescue of some features of Huntington Disease in the genetic absence of caspase-6 in YAC128 mice

Absence of Behavioral Abnormalities and Neurodegeneration in vivo despite Widespread Neuronal Huntingtin Inclusions

Full length mutant huntingtin is required for altered Ca2+ signaling and apoptosis of striatal neurons in the YAC mouse model of Huntington's disease

Accumulation of N-terminal mutant huntingtin in mouse and monkey models implicated as a pathogenic mechanism in Huntington's disease

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

Transgenic mouse model expressing the caspase 6 fragment of mutant huntingtin

Phosphorylation of huntingtin reduces the accumulation of its nuclear fragments

NP03, a novel low-dose lithium formulation, is neuroprotective in the YAC128 mouse model of Huntington disease

Systematic interaction network filtering identifies CRMP1 as a novel suppressor of huntingtin misfolding and neurotoxicity

Elevated brain 3-hydroxykynurenine and quinolinate levels in Huntington disease mice

Wild‐type huntingtin protects neurons from excitotoxicity

Caspase Cleavage of Mutant Huntingtin Precedes Neurodegeneration in Huntington's Disease

Phenotypic abnormalities in the YAC128 mouse model of Huntington disease are penetrant on multiple genetic backgrounds and modulated by strain

Polyglutamine-Modulated Striatal Calpain Activity in YAC Transgenic Huntington Disease Mouse Model: Impact on NMDA Receptor Function and Toxicity

Specific olfactory deficit patterns observed in seniors and associated with cognitive decline

Caspase-6 and neurodegeneration

Olfactory Dysfunction Associated with Cognitive Decline in an Elderly Population

Striatal neuronal apoptosis is preferentially enhanced by NMDA receptor activation in YAC transgenic mouse model of Huntington disease

Amelioration of Cognitive and Olfactory System Deficits in APOE4 Transgenic Mice with DHA Treatment

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