Very Slow Retrograde and Wallerian Degeneration in the CNS of C57BL/Ola Mice

Perry, V.H.; Brown, Michael C.; Lunn, E. R.

doi:10.1111/j.1460-9568.1991.tb00815.x

Cited by 124 publications

(89 citation statements)

References 14 publications

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“…We found that administration of a CD200R1 agonist attenuated disease in a chronic MS model (66). Enhanced CD200 expression was associated with reduced Wallerian degeneration in the slow Wallerian degeneration (Wld s ) mouse (67), a spontaneously occurring mutant with the unique phenotype of protection against several forms of axonal injury (68)(69)(70)(71). In vitro, Wld s neuronal cultures were protected from microglia-induced neurotoxicity, which was abrogated by anti-CD200 antibody treatment (67).…”

Section: Immune Cells Involved In Neurodegenerationmentioning

confidence: 92%

CNS inflammation and neurodegeneration

Chitnis¹,

Weiner²

2017

Journal of Clinical Investigation

398

240

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Section: Immune Cells Involved In Neurodegenerationmentioning

confidence: 92%

CNS inflammation and neurodegeneration

Chitnis¹,

Weiner²

2017

Journal of Clinical Investigation

398

240

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“…Projections of central neurons are also protected after lesions of axonal fiber tracts in Wld s mice, including the perforant path of the hippocampal formation and optic nerve (Perry et al, 1991;Shi and Stanfield, 1996). Less evident is whether Wld is associated with neuronal preservation more generally in the central nervous system (Ludwin and Bisby, 1992).…”

mentioning

confidence: 97%

Neuroprotection after Transient Global Cerebral Ischemia in Wld^s Mutant Mice

Gillingwater

Haley

Ribchester

et al. 2004

J Cereb Blood Flow Metab

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Summary:The Wld s mouse mutant demonstrates a remarkable phenotype of delayed axonal and synaptic degeneration after nerve lesion. In this study, the authors tested the hypothesis that expression of Wld protein is neuroprotective in an in vivo mouse model of global cerebral ischemia. This model is associated with selective neuronal degeneration in specific brain regions such as the caudate nucleus and CA2 hippocampal pyramidal cell layer. The extent of neuronal damage was quantified in Wld s compared to wild-type mice after an identical episode of global cerebral ischemia. The results demonstrated a significant and marked reduction in the extent of neuronal damage in Wld s as compared to wild-type C57Bl/6 mice.In the caudate nucleus, Wld expression significantly reduced the percentage of ischemic neuronal damage after global ischemia (Wld s , 27.7 ± 16.8%; wild-type mice, 58.7 ± 32.3%; P ‫ס‬ 0.036). Similarly, in the CA2 pyramidal cell layer, there was a significant reduction of neuronal damage in the Wld s mice as compared to wild-type mice after ischemia (Wld s , 17.7 ± 23.0%; wild-type mice, 41.9 ± 28.0%; P < 0.023). Thus, these results clearly demonstrate that the Wld gene confers substantial neuroprotection after cerebral ischemia, and suggest a new role to that previously described for Wld s .

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“…The Wlds mutant mouse that overexpresses a slow Wallerian degeneration protein (WldS), a fusion protein composed of the N-terminal 70 amino acids of ubiquitination factor E4 linked to full-length Nmnat1 exhibits slow axonal Wallerian degeneration in response to nerve injury in the peripheral nervous system (PNS). This WldS fusion protein protects axons from degeneration initiated by a variety of insults both in vitro and in vivo (15)(16)(17). Further, it has been shown in multiple axonal injury paradigms that expression of Nmnat1 robustly protects axons in vitro and in vivo in the PNS (18)(19)(20).…”

mentioning

confidence: 99%

Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death

Verghese

Sasaki

Yang

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Hypoxic-ischemic (H-I) injury to the developing brain is a significant cause of morbidity and mortality in humans. Other than hypothermia, there is no effective treatment to prevent or lessen the consequences of neonatal H-I. Increased expression of the NAD synthesizing enzyme nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) has been shown to be neuroprotective against axonal injury in the peripheral nervous system. To investigate the neuroprotective role of Nmnat1 against acute neurodegeneration in the developing CNS, we exposed wild-type mice and mice overexpressing Nmnat1 in the cytoplasm (cytNmnat1-Tg mice) to a well-characterized model of neonatal H-I brain injury. As early as 6 h after H-I, cytNmnat1-Tg mice had strikingly less injury detected by MRI. CytNmnat1-Tg mice had markedly less injury in hippocampus, cortex, and striatum than wild-type mice as assessed by loss of tissue volume 7 d days after H-I. The dramatic protection mediated by cytNmnat1 is not mediated through modulating caspase3-dependent cell death in cytNmnat1-Tg brains. CytNmnat1 protected neuronal cell bodies and processes against NMDA-induced excitotoxicity, whereas caspase inhibition or B-cell lymphoma-extra large (Bcl-XL) protein overexpression had no protective effects in cultured cortical neurons. These results suggest that cytNmnat1 protects against neonatal HI-induced CNS injury by inhibiting excitotoxicity-induced, caspase-independent injury to neuronal processes and cell bodies. As such, the Nmnat1 protective pathway could be a useful therapeutic target for acute and chronic neurodegenerative insults mediated by excitotoxicity.

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Very Slow Retrograde and Wallerian Degeneration in the CNS of C57BL/Ola Mice

Cited by 124 publications

References 14 publications

CNS inflammation and neurodegeneration

CNS inflammation and neurodegeneration

Neuroprotection after Transient Global Cerebral Ischemia in Wld^s Mutant Mice

Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death

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Very Slow Retrograde and Wallerian Degeneration in the CNS of C57BL/Ola Mice

Cited by 124 publications

References 14 publications

CNS inflammation and neurodegeneration

CNS inflammation and neurodegeneration

Neuroprotection after Transient Global Cerebral Ischemia in Wlds Mutant Mice

Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death

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Neuroprotection after Transient Global Cerebral Ischemia in Wld^s Mutant Mice