Complement inhibition accelerates regeneration in a model of peripheral nerve injury

Ramaglia, Valeria; Tannemaat, Martijn R.; Kok, Maryla de; Wolterman, Ruud A.; Vigar, Miriam Ann; King, R. H. M.; Morgan, B. Paul; Baas, Frank

doi:10.1016/j.molimm.2009.09.019

Cited by 26 publications

(29 citation statements)

References 28 publications

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“…Specifically, it is still unclear whether it triggers chronic neurodegeneration or it is simply the epiphenomenon of underlying pathogenic responses to neuronal damage. Over the past decade, our group has collected evidence which support a protective role for complement inhibitors in axonal damage [8][9][10]13]. We demonstrated that both genetic and pharmacological inhibition of MAC formation protects the peripheral nerve from early axon loss after traumatic injury [9,10,148], and stimulates post-traumatic axonal regeneration and functional recovery [149].…”

Section: Therapeutical Targetsmentioning

confidence: 91%

“…Although studies to verify complement activation in repetitive mild TBI or in CTE are lacking, the proved neuropathological role of complement in severe TBI [50] , AD [51,52], prion disease [53], ALS [14,54] and traumatic peripheral nerve injury [9][10][11][12][13], makes complement a likely player also in the neuropathology of concussive injuries and CTE. Complement is a key component of innate immunity.…”

Section: Microscopic Neuropathological Changesmentioning

confidence: 99%

“…Our effort over the past 10 years has been directed to study the role of the complement cascade in the nervous system [8][9][10][11][12][13][14]. To date we have collected evidence which support a role for complement in microglia priming [8] as well as the protective role of inhibitors of complement activation in nerve damage [10,13].…”

Section: Introductionmentioning

confidence: 99%

“…To date we have collected evidence which support a role for complement in microglia priming [8] as well as the protective role of inhibitors of complement activation in nerve damage [10,13]. Therefore, in this chapter we focus on the complement system as a potential target for therapy to fight neurodegeneration.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Uncovering the Path to Neurodegeneration from Playingfield to Battlefield

Baas¹,

Ramaglia²

2014

Traumatic Brain Injury

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Section: Therapeutical Targetsmentioning

confidence: 91%

Section: Microscopic Neuropathological Changesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Uncovering the Path to Neurodegeneration from Playingfield to Battlefield

Baas¹,

Ramaglia²

2014

Traumatic Brain Injury

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“…Clinically, the positive effect of MLT on neuroma formation and nerve regeneration seems particularly attractive. 15,27 Using an experimental PNI model, Atik et al suggested that the powerful antioxidant and cell-protective effects of MLT could result from mimicking calcium channel blockers. 28 It is therefore believed that boosting peripheral nerve repair with MLT could be a worthwhile option, in addition to other treatment modalities, in cases of MLT deficiency.…”

Section: Free Radical Scavenging Effects Of Melatonin In Peripheral Nmentioning

confidence: 99%

Untitled

2017

J Brachial Plex Peripher Nerve Inj

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Aging of myelinating glial cells predominantly affects lipid metabolism and immune response pathways

Csárdi

Preux-Charles

Médard

et al. 2012

Glia

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Both the central and the peripheral nervous systems are prone to multiple age-dependent neurological deficits, often attributed to still unknown alterations in the function of myelinating glia. To uncover the biological processes affected in glial cells by aging, we analyzed gene expression of the Schwann cell-rich mouse sciatic nerve at 17 time points throughout life, from day of birth until senescence. By combining these data with the gene expression data of myelin mouse mutants carrying deletions of either Pmp22, SCAP, or Lpin1, we found that the majority of age-related transcripts were also affected in myelin mutants (54.4%) and were regulated during PNS development (59.5%), indicating a high level of overlap in implicated molecular pathways. The expression profiles in aging copied the direction of transcriptional changes observed in neuropathy models; however, they had the opposite direction when compared with PNS development. The most significantly altered biological processes in aging involved the inflammatory/immune response and lipid metabolism. Interestingly, both these pathways were comparably changed in the aging optic nerve, suggesting that similar biological processes are affected in aging of glia-rich parts of the central and peripheral nervous systems. Our comprehensive comparison of gene expression in three distinct biological conditions including development, aging, and myelin disease thus revealed a previously unanticipated relationship among themselves and identified lipid metabolism and inflammatory/immune response pathways as potential therapeutical targets to prevent or delay so far incurable age-related and inherited forms of neuropathies.

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Complement inhibition accelerates regeneration in a model of peripheral nerve injury

Cited by 26 publications

References 28 publications

Uncovering the Path to Neurodegeneration from Playingfield to Battlefield

Uncovering the Path to Neurodegeneration from Playingfield to Battlefield

Untitled

Aging of myelinating glial cells predominantly affects lipid metabolism and immune response pathways

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