Citicoline and lithium rescue retinal ganglion cells following partial optic nerve crush in the rat

Schuettauf, Frank; Ręjdak, Robert; Thaler, Sebastian; Bolz, Sylvia; Lehaci, Cristiana; Mańkowska, Anna; Żarnowski, Tomasz; Jünemann, Anselm; Zagórski, Z; Zrenner, Eberhart; Grieb, Paweł

doi:10.1016/j.exer.2006.05.021

Cited by 80 publications

(52 citation statements)

References 27 publications

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“…For immunohistochemistry, retinal sections of animals aged 3, 6 and 11 months (n=10 each for both DBA/2J and C57BL/6 mice) were prepared, stained and recorded as described in detail previously [50,53].…”

Section: Immunohistochemistrymentioning

confidence: 99%

Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration

Schuettauf

Thaler

Bolz

et al. 2007

Graefes Arch Clin Exp Ophthalmol

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Section: Immunohistochemistrymentioning

confidence: 99%

Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration

Schuettauf

Thaler

Bolz

et al. 2007

Graefes Arch Clin Exp Ophthalmol

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“…Our earlier study showed that citicoline had a neuroprotective effect on damaged RGCs and supported neurite regeneration in vitro [111]. Other groups demonstrated the protective effects of citicoline for RGCs in vivo animal models [121,122]. A more recent study showed that intramuscular injections of citicoline significantly improved the electroretinograms and visual evoked cortical potentials in glaucoma patients during an 8-year follow-up period [123].…”

Section: Neurotrophic Factorsmentioning

confidence: 99%

Diabetes Mellitus and Retinal Vein Occlusion as Risk Factors for Open Angle Glaucoma and Neuroprotective Therapies for Retinal Ganglion Cell Neuropathy

Bikbova¹,

Oshitari²,

Yamamoto³

2011

J Clin Exp Ophthalmol

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of glaucoma (NTG), and the prevalence of NTG is 3.6% in patients >40-years-of-age in Japan [10]. The average intraocular pressure (IOP) in patients with POAG is 15.4 ± 2.8 mmHg, which is significantly higher than that of normal subjects (14.5 ± 2.5 mmHg) [1][2][3][4][5][6][7][8][9][10] even though the average difference in the IOP is only 0.9 mmHg. Thus, a reduction of the IOP the standard therapy for glaucoma may not be sufficient for the complete management of the patients with glaucoma in Japan. Other therapeutic modalities, such as neuroprotection, should be considered for a complete therapeutic regimen for glaucoma patients.RGC death and axonal degeneration are most likely involved in the progression of DR, RVO, and glaucoma. Many neuroprotective therapies that prevent RGC death and axonal degeneration have been and are being investigated, and some of these neuroprotective factors may be used clinically in the near future. To establish neuroprotective therapies for DR, RVO and glaucoma, a determination of the exact mechanism that leads to a progression of RGC neuropathy to death and axonal degeneration is required [11]. However, the pathogenesis of the onset and progression of RGC neuropathy has still not been definitively determined. Identification of the risk factors for the onset and the progression of disease would help in determining the Abstract Glaucoma, diabetic retinopathy (DR), and retinal vein occlusion (RVO) are major diseases that can lead to blindness and affect mainly the elderly population worldwide. The results of recent investigations have demonstrated that the death of retinal ganglion cells (RGCs) and their axons is the common pathological change in these three disease processes. The exact mechanism that is responsible for the onset and progression of RGC death and axonal degeneration in patients with glaucoma, DR and RVO has not been definitively determined. Thus, identifying the risk factors for the onset and the progression of RGC neuropathy can help in deciding not only the specific treatments but also whether the treatments should be initiated, withheld, or augmented in individuals with glaucoma, DR, and RVO. This review describes the major risk factors for the onset of glaucoma, and the factors associated with the progression of glaucoma that have been obtained from large population-based prevalence and incidence studies. In addition, the potential risk factors for glaucoma, diabetes mellitus, and RVO are discussed in terms of the results obtained by both clinical and laboratory studies. This review introduces potential neuroprotective therapies for damaged RGC in eyes with RGC neuropathy, and the factors that should be considered for a complete therapy for the RGC neuropathy involved in glaucoma, DR and RVO. Neuroprotective therapies combined with a reduction of the IOP should be considered for the complete management of RGC neuropathy involved in glaucoma,

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“…In recent years, accumulating evidence demonstrated that lithium is a robust neuroprotective agent for certain central neurons [1,2,3,4,5,6,7,8]. In the visual system, lithium promotes the survival of either retinal ganglion cells (RGCs) in vitro and axotomized RGCs in vivo after optic nerve (ON) crush in adult mice and rats [9,10,11]. Such protective effects of lithium have been attributed to upregulated expression of Bcl-2 in RGCs [9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Dose-Dependent Protective Effect of Lithium Chloride on Retinal Ganglion Cells Is Interrelated with an Upregulated Intraretinal BDNF after Optic Nerve Transection in Adult Rats

Zhu

Wang

et al. 2014

IJMS

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Neuroprotection of lithium for axotomized retinal ganglion cells (RGCs) is attributed to upregulated intraretinal Bcl-2. As lithium also upregulates brain-derived neurotrophic factor (BDNF) which can rescue axotomized RGCs, it is hypothesized that lithium could protect RGCs through BDNF. This study investigated this hypothesis and a possible relationship between the dose and protection of lithium. All adult experimental rats received daily intraperitoneal injections of lithium chloride (LiCl) at 30, 60 or 85 mg/kg·bw until they were euthanized 2, 7 or 14 days after left intraorbital optic nerve (ON) transection. Our results revealed that RGC densities promoted and declined with increased dose of LiCl and the highest RGC densities were always in the 60 mg/kg·bw LiCl group at both 7 and 14 day points. Similar promotion and decline in the mRNA and protein levels of intraretinal BDNF were also found at the 14 day point, while such BDNF levels increased in the 30 mg/kg·bw LiCl group but peaked in the 60 and 85 mg/kg·bw LiCl groups at the 7 day point. These findings suggested that lithium can delay the death of axotomized RGCs in a dose-dependent manner within a certain period after ON injury and such beneficial effect is interrelated with an upregulated level of intraretinal BDNF.

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Citicoline and lithium rescue retinal ganglion cells following partial optic nerve crush in the rat

Cited by 80 publications

References 27 publications

Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration

Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration

Diabetes Mellitus and Retinal Vein Occlusion as Risk Factors for Open Angle Glaucoma and Neuroprotective Therapies for Retinal Ganglion Cell Neuropathy

Dose-Dependent Protective Effect of Lithium Chloride on Retinal Ganglion Cells Is Interrelated with an Upregulated Intraretinal BDNF after Optic Nerve Transection in Adult Rats

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