2007
DOI: 10.1016/j.neubiorev.2007.04.015
|View full text |Cite
|
Sign up to set email alerts
|

Synaptic dysfunction in disease and following injury in the developing and adult nervous system: Caveats in the choice of therapeutic intervention☆

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
16
0

Year Published

2009
2009
2016
2016

Publication Types

Select...
6
1

Relationship

0
7

Authors

Journals

citations
Cited by 13 publications
(17 citation statements)
references
References 204 publications
(192 reference statements)
1
16
0
Order By: Relevance
“…These observations are consistent with the report of spontaneous Wallerian-like degeneration of the neurites of cultured sympathetic ganglia neurons that occurs in a dying-back proximal-distal pattern following knock-down of Nmnat2 [8]. Thus, endogenous Nmnat2 may play a critical role in the stabilization (maintenance) of peripheral axons and the prevention of axonal regression [1], [29], [30].…”
Section: Discussionsupporting
confidence: 91%
“…These observations are consistent with the report of spontaneous Wallerian-like degeneration of the neurites of cultured sympathetic ganglia neurons that occurs in a dying-back proximal-distal pattern following knock-down of Nmnat2 [8]. Thus, endogenous Nmnat2 may play a critical role in the stabilization (maintenance) of peripheral axons and the prevention of axonal regression [1], [29], [30].…”
Section: Discussionsupporting
confidence: 91%
“…Recent evidence derived from the study of animal models of various neuropathological conditions has revealed that damage to axons and synapses often long precedes the activation of death pathways and the onset of clinical (i.e., functional) pathology (Raff et al 2002; Medana and Esiri 2003; Palop et al 2006; Gould and Oppenheim 2007). In the case of mouse models of ALS, muscle denervation occurs months before MN death or disease onset (Frey et al 2000; Fischer et al 2004; Gould et al 2006; Pun et al 2006).…”
Section: Literature Reviewmentioning
confidence: 99%
“…The impairment of axonal transport in SOD1 mice has been attributed to appearance of neurofilament (NF) inclusions in mutant axons (Zhang et al 1997), but mutations in transport proteins in the dynein/dynactin complex also occur (LaMonte et al 2002; Hafezparast et al 2003; Puls et al 2003). The enrichment within neurons of mitochondria near sites of activity such as axons, dendrites, and presynaptic terminals indicates that mitochondrial localization may be the target of disease toxicity in fALS as well as in other neurodegenerative diseases involving distal-to-proximal axonal pathology (Gould and Oppenheim 2007). It is an attractive possibility that altered transport of either normal or defective mitochondria to and/or from MN presynaptic terminals contributes to neuromuscular denervation and MN disease (but see, Marinkovic et al 2012).…”
Section: Literature Reviewmentioning
confidence: 99%
See 1 more Smart Citation
“…Thus, it may be speculated that the exposure of classical MHC class I molecules loaded with "self" or "non-self" peptides on peripheral motor axons may induce an immune response with adverse effects on motoneurons. This, in turn, is of interest in relation to the emerging focus on axonal and synaptic pathology as early signs and even as key triggering factors for the onset of neurodegenerative disease (Raff et al, 2002;Selkoe, 2002;Conforti et al, 2007;Gould and Oppenheim, 2007;Saxena and Caroni, 2007). In this context, it is of interest that MHC class I mRNA has been detected in all peripheral motoneuron groups, except for the ocular motor nuclei, which are known to be spared in the motoneuron neurodegenerative disorder amyotrophic lateral sclerosis (Lindå et al, 1999).…”
Section: Mhc Class Ia Proteins and Nmj Plasticitymentioning
confidence: 99%