New calpain inhibitor preserves brain architecture in 3‐nitropropionic acid (3‐NP) model of Huntington disease

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Brain networks in Huntington disease.

Recent studies have focused on understanding the neural mechanisms underlying the emergence of clinical signs and symptoms in early stage Huntington disease (HD). Although cell-based assays have focused on cell autonomous effects of mutant huntingtin, animal HD models have revealed alterations in the function of neuronal networks, particularly those linking the cerebral cortex and striatum. The...

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Calpain facilitates the neuron death induced by 3-nitropropionic acid and contributes to the necrotic morphology.

3-Nitropropionic acid (3NP), an irreversible inhibitor of succinate dehydrogenase, has been used to model features of neurodegenerative disorders including Huntington disease, as well as acute neuronal insults such as cerebral ischemia. 3NP induces rapid necrosis and delayed apoptosis in primary cultures of rat hippocampal neurons. Low levels of extracellular glutamate shift the cell death mech...

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Background & Aim: Parkinson's disease (PD) can be created with loss of dopaminergic substantial nigra neurons which is widely associated with oxidative stress and reduced glutathione (GSH), as the most important and abundant thiol in tissues and one of the antioxidant defense, is one of the earliest biochemical events related to Parkinson's and consumption of antioxidants has a protective effec...

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Effect of ellagic acid on thiol levels in different brain tissue in an animal model of Parkinson's disease

Background & Aim: Parkinson's disease (PD) can be created with loss of dopaminergic substantial nigra neurons which is widely associated with oxidative stress and reduced glutathione (GSH), as the most important and abundant thiol in tissues and one of the antioxidant defense, is one of the earliest biochemical events related to Parkinson's and consumption of antioxidants has a protective effec...

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ژورنال

عنوان ژورنال: The FASEB Journal

سال: 2009

ISSN: 0892-6638,1530-6860

DOI: 10.1096/fasebj.23.1_supplement.675.7