Nrf2 defense pathway: Experimental evidence for its protective role in epilepsy

Mazzuferi, Manuela; Kumar, Gaurav; Eyll, Jonathan van; Danis, Bénédicte; Foerch, Patrik; Kamiński, Rafał M.

doi:10.1002/ana.23940

Cited by 121 publications

(119 citation statements)

References 44 publications

Supporting

Mentioning

115

Contrasting

Unclassified

Order By: Relevance

“…Likewise in the liver, nuclear extracts demonstrated increased Nrf2 expression after 1 and 3 weeks on the diet, accompanied by elevations in both NAD(P)H:quinone oxidoreductase activity and the expression of Nrf2 target heme oxygenase-1 after 3 weeks on the diet ( 97 ). Interestingly, a recent study found that increasing Nrf2 expression in a rat model of temporal lobe epilepsy decreased spontaneous seizures ( 100 ).…”

Section: Bioenergetic and Mitochondrial Changesmentioning

confidence: 98%

Ketogenic diets, mitochondria, and neurological diseases

Gano

Patel

Rho

2014

Journal of Lipid Research

214

193

View full text Add to dashboard Cite

Section: Bioenergetic and Mitochondrial Changesmentioning

confidence: 98%

Ketogenic diets, mitochondria, and neurological diseases

Gano

Patel

Rho

2014

Journal of Lipid Research

214

193

View full text Add to dashboard Cite

“…Systems biology-based approaches of network pharmacology have recently been proposed for developing antiepileptic and antiepileptogenic treatments [4,50,51]. In addition to combining drugs in network pharmacology, one target that modulates several pathways is an alternative option as illustrated by the mTOR pathway [52] or transcription factors such as Nrf2 [53].…”

Section: Concept Of Network Pharmacologymentioning

confidence: 99%

Searching for the Ideal Antiepileptogenic Agent in Experimental Models: Single Treatment Versus Combinatorial Treatment Strategies

White

Löscher²

2014

Neurotherapeutics

View full text Add to dashboard Cite

A major unmet medical need is the lack of treatments to prevent (or modify) epilepsy in patients at risk, for example, after epileptogenic brain insults such as traumatic brain injury, stroke, or prolonged acute symptomatic seizures like complex febrile seizures or status epilepticus. Typically, following such brain insults there is a seizure-free interval ("latent period"), lasting months to years before the onset of spontaneous recurrent epileptic seizures. The latent period after a brain insult offers a window of opportunity in which an appropriate treatment may prevent or modify the epileptogenic process induced by a brain insult. A similar latent period occurs in patients with epileptogenic gene mutations. Studies using animal models of epilepsy have led to a greater understanding of the factors underlying epileptogenesis and have provided significant insight into potential targets by which the development of epilepsy may be prevented or modified. This review focuses largely on some of the most common animal models of epileptogenesis and their potential utility for evaluating proposed antiepileptogenic therapies and identifying useful biomarkers. The authors also describe some of the limitations of using animal models in the search for therapies that move beyond the symptomatic treatment of epilepsy. Promising results of previous studies designed to evaluate antiepileptogenesis and the role of monotherapy versus polytherapy approaches are also discussed. Recent data from both models of genetic and acquired epilepsies strongly indicate that it is possible to prevent or modify epileptogenesis, and, hopefully, such promising results can ultimately be translated into the clinic.

show abstract

“…Both groups of antioxidant genes have been proposed as therapeutic candidates, e.g., for neurodegenerative disorders, diabetic complications, and cardiovascular diseases, with the hope that the enzymes would be more specific, generating fewer side effects than chemical antioxidants, and that the TFs would provide a broad defense by activating hundreds of genes (15)(16)(17). However, only a few studies have been conducted to test this therapeutic strategy by gene delivery via viral vectors in animal models in vivo (18)(19)(20)(21)(22)(23)(24)(25), and no studies have compared the effectiveness of the enzymes versus the TFs, or NRF2 versus PGC1a.…”

Section: Introductionmentioning

confidence: 99%