These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Soluble amyloid beta oligomers may contribute to apoptosis of retinal ganglion cells in glaucoma.
    Author: Yin H, Chen L, Chen X, Liu X.
    Journal: Med Hypotheses; 2008; 71(1):77-80. PubMed ID: 18406539.
    Abstract:
    Glaucoma is one of the leading causes of visual impairment and blindness. It is characterized by excavation of optic nerve head and visual field loss. Even though the pathogenesis of glaucoma remains unclear, it is generally accepted that elevated intraocular pressure is the major risk factor. No matter what the specific initiators are, retinal ganglion cells are believed to die via apoptosis eventually. It is known that glaucoma correlates strongly with Alzheimer's disease and the two diseases share many similarities in pathogenic mechanisms. Recent studies have indicated that amyloid beta peptide, which is implicated in the progression of Alzheimer's disease, may be also responsible for retinal ganglion cells death in glaucoma. Amyloid beta exists in different forms, including monomers, oligomers and fibrils, and among these, as demonstrated by extensive evidences, soluble amyloid beta oligomers rather than insoluble amyloid beta fibrils induced apoptosis of neurons in Alzheimer's disease. Here we propose that soluble amyloid beta oligomers may play an important role in activation of apoptotic cascades in retinal ganglion cells in glaucoma.
    [Abstract] [Full Text] [Related] [New Search]