The neuropeptide NAP provides neuroprotection against retinal ganglion cell damage after retinal ischemia and optic nerve crush

Jehle, Thomas; Dimitriu, C; Auer, Stefanie; Knoth, Rolf; Vidal‐Sanz, Manuel; Gozes, Illana; Lagrèze, Wolf A.

doi:10.1007/s00417-007-0746-7

Cited by 61 publications

(44 citation statements)

References 48 publications

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“…We have further identified NAP (davunetide) as a neurotrophic factor, stimulating neurite outgrowth and synapse formation [138]. These results were corroborated by other investigators worldwide [104,139,140].…”

Section: H 2 N-asn-ala-pro-val-ser-ile-pro-gln-coohsupporting

confidence: 82%

Tau Pathology and Future Therapeutics

Gozes

2010

CAR

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The current review discusses microtubules and tau in the healthy brain and move on to the underling pathology of Alzheimer's disease (AD) with emphasis on tau and neurofibrillary tangles. Tangles have been associated with cognitive dysfunction causing neurodegeneration in the absence of plaques. AD, the most abundant tauopathy is characterized by β-amyloid plaques and tau tangles. An abundance of tau inclusions, in the absence of β-amyloid deposits, defines Pick's disease (frontotemporal lobar degeneration), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and other diseases. Our own focused research is on activity-dependent neuroprtective protein (ADNP). Our findings show that ADNP-deficiency leads to tauopathy which is inhibited by the ADNP derived drug candidate, davunetide (originally known as NAP). The current review further describes tau as a potential diagnostic marker followed by drug candidates that are aimed at fighting tau pathology. A recent historical perspective is the final comment of the manuscript. This paper is not a comprehensive review of the literature rather it gives my own point of view in the face of many publications and a great unmet need for future therapeutics. It is hoped that davunetide, a most advanced drug in clinical development will rapidly advance as a first effective treatment for a number of brain disorders broadly categorized as frontotemporal dementia (FTD) and serve as a prototype for future therapeutic development toward modification and remedy of currently intractable neurodegenerative diseases.

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Section: H 2 N-asn-ala-pro-val-ser-ile-pro-gln-coohsupporting

confidence: 82%

Tau Pathology and Future Therapeutics

Gozes

2010

CAR

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“…This has prompted investigators to look for alternatives to prevent or slow cell death using neuroprotective drugs (Almasieh et al, 2012;Nucci et al, 2013b;Russo et al, 2013). Partial and transient rescue of RGCs against a variety of retinal injuries has been shown with several neuroprotective agents ( Jehle et al, 2008;Vidal-Sanz et al, 2000, 2001, including brain-derived neurotrophic factor (BDNF), which has been shown to be one of the most potent RGC neuroprotectants (Di Polo et al, 1998;Galindo-Romero et al, 2013b;Mansour-Robaey et al, 1994;Peinado-Ramón et al, 1996;Sánchez-Migallón et al, 2011). Indeed, the administration of BDNF has been shown to prevent OHT-induced RGC loss (Almasieh et al, 2012;Di Polo et al, 1998;Fu et al, 2009;Ko et al, 2001;Lebrun-Julien et al, 2008;Martin et al, 2003;Quigley et al, 2000;Wilson and Di Polo, 2012).…”

Section: Introductionmentioning

confidence: 99%

Retinal neurodegeneration in experimental glaucoma

Vidal‐Sanz

Valiente‐Soriano

Ortín-Martínez

et al. 2015

Progress in Brain Research

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“…The responses of RGCs to optic nerve injury have been studied extensively (Vidal-Sanz et al, 2000, 2007; Lindqvist et al, 2004; Jehle et al, 2008; Parrilla-Reverter et al, 2009a,b). Indeed, complete intraorbital optic nerve crush (ONC) or transection (ONT) are clean and reproducible models with relatively little inter-animal variability (Vidal-Sanz et al, 1987; Peinado-Ramón et al, 1996; Sobrado-Calvo et al, 2007; Parrilla-Reverter et al, 2009a; Sánchez-Migallón et al, 2011, 2016; Nadal-Nicolás et al, 2015a; Rovere et al, 2016a).…”

Section: Introductionmentioning

confidence: 99%

Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

et al. 2017

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Glaucoma, one of the leading causes of blindness worldwide, affects primarily retinal ganglion cells (RGCs) and their axons. The pathophysiology of glaucoma is not fully understood, but it is currently believed that damage to RGC axons at the optic nerve head plays a major role. Rodent models to study glaucoma include those that mimic either ocular hypertension or optic nerve injury. Here we review the anatomical loss of the general population of RGCs (that express Brn3a; Brn3a+RGCs) and of the intrinsically photosensitive RGCs (that express melanopsin; m+RGCs) after chronic (LP-OHT) or acute (A-OHT) ocular hypertension and after complete intraorbital optic nerve transection (ONT) or crush (ONC). Our studies show that all of these insults trigger RGC death. Compared to Brn3a+RGCs, m+RGCs are more resilient to ONT, ONC, and A-OHT but not to LP-OHT. There are differences in the course of RGC loss both between these RGC types and among injuries. An important difference between the damage caused by ocular hypertension or optic nerve injury appears in the outer retina. Both axotomy and LP-OHT induce selective loss of RGCs but LP-OHT also induces a protracted loss of cone photoreceptors. This review outlines our current understanding of the anatomical changes occurring in rodent models of glaucoma and discusses the advantages of each one and their translational value.

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The neuropeptide NAP provides neuroprotection against retinal ganglion cell damage after retinal ischemia and optic nerve crush

Abstract: NAP acts neuroprotectively in vivo after retinal ischemia and optic nerve crush, and may have potential in treating optic nerve diseases.

Cited by 61 publications

References 48 publications

Tau Pathology and Future Therapeutics

Tau Pathology and Future Therapeutics

Retinal neurodegeneration in experimental glaucoma

Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

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