Apoptosis related antigen, Le Y and nick-end labeling are positive in spinal motor neurons in amyotrophic lateral sclerosis

Yoshiyama, Yasumasa; Yamada, Toyo Kazu; Asanuma, Katsumi; Asahi, Toshiomi

doi:10.1007/s004010050151

Cited by 28 publications

(28 citation statements)

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“…Several groups have demonstrated the presence of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive staining in muscle cells (Tews et al, 1997) and in spinal cord motor neurons (Yoshiyama et al, 1994) of ALS patients but not in controls. Expression of several different ALS-linked SOD1 protein mutants in cultured neuronal cells resulted in apoptotic cell death (as judged by TUNEL staining), whereas expression of wild-type SOD1 conferred protection from apoptosis (Rabizadeh et al, 1995;Durham et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Bcl-2 Overexpression Does Not Protect Neurons from Mutant Neurofilament-Mediated Motor Neuron Degeneration

Houseweart¹,

Cleveland²

1999

J. Neurosci.

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Transgenic mice with a point mutation in the light neurofilament gene develop amyotrophic lateral sclerosis–like motor neuron disease characterized by selective spinal motor neuron loss, neurofilamentous accumulations, and severe muscle atrophy. To test whether the large motor neurons at risk in this disease could be protected from mutant neurofilament-mediated killing, these mice were bred to mice overexpressing the humanBcl-2proto-oncogene. Elevated levels of Bcl-2 increased the numbers of motor and sensory axons surviving after the developmental period of naturally occurring cell death but did not greatly reduce the number of degenerating axons or protect the large motor neurons from mutant neurofilament-mediated death.

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Section: Discussionmentioning

confidence: 99%

Bcl-2 Overexpression Does Not Protect Neurons from Mutant Neurofilament-Mediated Motor Neuron Degeneration

Houseweart¹,

Cleveland²

1999

J. Neurosci.

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“…In addition to this caveat, the search for DNA fragmentation in ALS postmortem samples has generated conflicting results. In one autopsy study, DNA fragmentation was detected by an in situ method in spinal cord motor neurons in ALS but not in control specimens (39). In two other similar studies, DNA fragmentation was detected not only in the motor cortex and spinal cord of ALS specimens, but also, though to a lesser degree, in control specimens (40,41).…”

Section: Expression Of Apoptotic Markersmentioning

confidence: 95%

Programmed cell death in amyotrophic lateral sclerosis

Guégan¹,

Przedborski²

2003

J. Clin. Invest.

126

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“…Evidence has been presented for apoptotic neuronal cell death in stroke (Linnik et al, 1993), Parkinson's disease (Mochizuki et al, 1996), Alzheimer's disease (Cotman and Anderson, 1995), amyotrophic lateral sclerosis (AL S) (Yoshiyama et al, 1994), human immunodeficiency virus encephalopathy (Gelbard et al, 1995), cerebral trauma (Rink et al, 1995), Huntington's disease (Dragunow et al, 1995), and other diseases (Bredesen, 1994).…”

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confidence: 99%

Establishment of a Cell-Free System of Neuronal Apoptosis: Comparison of Premitochondrial, Mitochondrial, and Postmitochondrial Phases

et al. 1997

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Apoptosis is a fundamental process required for normal development of the nervous system and is triggered during neurodegenerative disease. To dissect the molecular events leading to neuronal cell death, we have developed a cell-free model of neuronal apoptosis. The model faithfully reproduces key elements of apoptosis, including chromatin condensation, DNA fragmentation, caspase activation/processing, and selective substrate cleavage. We report that cell-free apoptosis is activated in premitochondrial, mitochondrial, and postmitochondrial phases by tamoxifen, mastoparan, and cytochrome c, respectively, allowing a functional ordering of these proapoptotic modulators. Furthermore, this is the first report of mitochondrial-mediated activation of cell-free apoptosis in a cell extract. Although Bcl-2 blocks activation at the premitochondrial and mitochondrial levels, it does not affect the postmitochondrial level. The cell-free system described here provides a valuable tool to elucidate the molecular events leading to neuronal cell death.

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Apoptosis related antigen, Le Y and nick-end labeling are positive in spinal motor neurons in amyotrophic lateral sclerosis

Cited by 28 publications

References 0 publications

Bcl-2 Overexpression Does Not Protect Neurons from Mutant Neurofilament-Mediated Motor Neuron Degeneration

Bcl-2 Overexpression Does Not Protect Neurons from Mutant Neurofilament-Mediated Motor Neuron Degeneration

Programmed cell death in amyotrophic lateral sclerosis

Establishment of a Cell-Free System of Neuronal Apoptosis: Comparison of Premitochondrial, Mitochondrial, and Postmitochondrial Phases

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