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Journal of Biochemical and Pharmacological Research

ISSN 2168-8761 (Print)

ISSN 2168-877X (Online)

Website: http://www.researchpub.org/journal/jbpr/jbpr.html

Open special issues

Special Issue on Age-related macular degeneration (AMD)

Call for Papers

Age-related macular degeneration (AMD) is a complex, degenerative and progressive eye disease that results in severe loss of central vision. Risk factors for AMD include age, genetics, diet, smoking, oxidative stress, arteriosclerosis, hypertension, hypercholesterolemia and unhealthy diet. The macula is a highly specialized region of the central retina unique to humans and other primates that is normally responsible for achieving high acuity and color vision. Patients suffering AMD have difficulty in seeing letters on a page, reduced ability to distinguish contrasts, distortion of straight lines, central visual field defects, scotomas and color vision impairment. AMD is the most common cause of visual impairment in Western countries. Worldwide, approximately 50 million elderly people suffer from AMD, and the number of cases is expected to rise 3-fold over the next 20 years, suggesting that AMD is becoming a major public health issue.

Degenerative tissue alterations that occur at the interface between the neural retina including rod and cone photoreceptors, retinal pigment epithelial (RPE) cells, Bruch´s membrane and the underlying choroid contribute to the pathology of AMD. Phenotypically, AMD can be divided into two main forms: dry (atrophic, 85 % of all AMD cases) and wet (exudative, 15 %) type and further subdivided into early and late stage disease. A hallmark of AMD is the detrimental accumulation of lysosomal lipofuscin in the postmitotic RPE cells. Moreover, the presence of extracellular drusen deposits between the basal lamina of the RPE and the Bruch’s membrane are common in AMD. To date, there is increasing evidence that constant oxidative stress, chronic inflammation and impaired protein clearance via proteasomes, lysosomes or autophagy and increased protein aggregation evoke the pathological phenotype of AMD.

Now, we invite researchers and scientists to contribute original research- as well as review articles that will encourage continuing attempts and endeavours to understand not only the pathophysiology of AMD but also expand the knowledge and strategies to treat or prevent the process of the disease. In particular, articles describing the new finding on the role of oxidative stress, inflammation, protein aggregation and clearance in initiation and development of AMD are welcome. Potential topics include, but are not limited to:

  • Oxidative stress and innate immunity response in retinal and choroidal cells
  • Function of molecular chaperones in proteolysis
  • Molecular mechanisms for proteasomal, lysosomal and autophagy clearance
  • Regulation of neovascularisation process in retinal and choroidal cells
  • Novel cell culture and animal models to study AMD pathology
  • Novel biomarkers for AMD
  • Deadline of submission: Feb. 1, 2014.

    All articles will be published in the first issue of 2014 as Volume 2, issue 1. Authors should follow the submission guidelines located at: http://researchpub.org/journal/jbpr/author%20guidelines.html

    Lead Guest Editor

    Kai Kaarniranta, Department of Ophthalmology; University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland; kai.kaarniranta@uef.fi

    Guest Editors

    Anna Machalinska, Department of Histology and Embryology, Pomeranian Medical University, Szczecin, Poland; annam@sci.pam.szczecin.pl

    Goran Petrovski, Department of Ophthalmology; University of Szeged, Szeged, Hungary, petrovski.goran@med.u-szeged.hu