Induction of nitrotyrosine-like immunoreactivity in the lower motor neuron of amyotrophic lateral sclerosis☆
References (22)
- et al.
Familial amyotrophic lateral sclerosis (ALS) in Japan associated with H46R mutation in Cu/Zn superoxide dismutase gene: a possible new subtype of familial ALS
J. Neurol. Sci.
(1994) - et al.
Oxygen radicals and the nervous system
Trends Neurosci.
(1985) - et al.
A novel mutation in Cu/Zn superoxide dismutase gene in Japanese familial amyotrophic lateral sclerosis
Biochem. Biophys. Res. Commun.
(1994) - et al.
Amyotrophic lateral sclerosis associated with homozygosity for an Asp90Ala mutation in CuZn-superoxide dismutase
Nat. Genet.
(1995) - et al.
Mild ALS in Japan associated with novel SOD mutation
Nat. Genet.
(1993) - et al.
ALS, SOD and peroxynitrite
Nature
(1993) - et al.
Amyotrophic lateral sclerosis and structural defects in Cu/Zn superoxide dismutase
Science
(1993) - et al.
Two novel SOD1 mutations in patients with familial amyotrophic lateral sclerosis
Hum. Mol. Genet.
(1995) - et al.
Identification of a new missense point mutation in exon 4 of the Cu/Zn superoxide dismutase (SOD-1) gene in a family with amyotrophic lateral sclerosis
Hum. Mol. Genet.
(1994) - et al.
Two novel mutations in the gene for copper zinc superoxide dismutase in UK families with amyotrophic lateral sclerosis
Hum. Mol. Genet.
(1995)
Identification of two novel mutations and a new polymorphism in the gene for Cu/Zn superoxide dismutase in patients with amyotrophic lateral sclerosis
Hum. Mol. Genet.
Cited by (231)
Posttranslational modifications of TDP-43
2022, TDP-43 and Neurodegeneration: From Bench to BedsideAssessment of neuroprotective effects of Gallic acid against glutamate-induced neurotoxicity in primary rat cortex neuronal culture
2018, Neurochemistry InternationalCitation Excerpt :Here, we studied the neuroprotective effects of GA against glutamate-induced neurotoxicity in primary neuronal cultures of neonatal rat cortex neurons and GA is proved to have a significant effect in protecting neurons from glutamate toxicity. The generation of ROS and its involvement in the pathogenesis of ALS was well implemented (Abe et al., 1997, 1995). Hence, the studies suggest that the oxidative stress as primary pathogenesis behind neurodegenerative diseases.
The interplay between inflammation, oxidative stress, DNA damage, DNA repair and mitochondrial dysfunction in depression
2018, Progress in Neuro-Psychopharmacology and Biological PsychiatryIn vivo EPR pharmacokinetic evaluation of the redox status and the blood brain barrier permeability in the SOD1<sup>G93A</sup> ALS rat model
2017, Free Radical Biology and MedicineGene Therapy for Amyotrophic Lateral Sclerosis: Therapeutic Transgenes
2017, Molecular and Cellular Therapies for Motor Neuron DiseasesTherapeutic progress in amyotrophic lateral sclerosis-beginning to learning
2016, European Journal of Medicinal ChemistryCitation Excerpt :However, it did not evoke any reversal of motor deterioration [51]. Oxidative damage has been studied in cellular and rodent models of ALS [52,53], in spinal cord and motor cortex motor neurons [54,55], in post mortem tissue of ALS patients [56,57] and in CSF of ALS patients [58,59]. Several neuroprotective agents with antioxidant abilities have been studied in connection to ALS and here we summarize some of them (Table 1).
- ☆
This work was partly supported by Grant-in-Aid for Scientific Research on Priority Areas (Kanazawa I) 06272204,and 07264204, and Grant-in-Aid for Scientific Research (B) 07457152 and (C) 06807055 from the Ministry of Education, Science and Culture of Japan, and by a grant (Hirai S) from the Ministry of Health and Welfare of Japan.
- ∗
The authors appreciate cooperation of the patients and their families with this project. We thank J.S. Beckman, T. Siddique, and RH. Brown Jr. for the generous discussion and support.