Glaucoma: thinking in new ways-a rôle for autonomous axonal self-destruction and other compartmentalised processes? Export

@article{citeulike:1567272, abstract = {Glaucoma is a common neurodegenerative disease that affects retinal ganglion cells (RGCs). Substantial effort is being expended to determine how RGCs die in glaucoma. As in other neurodegenerative diseases, the majority of effort focuses on characterising apoptotic self-destruct pathways. However, apoptosis is not the only self-destruct mechanism that may be activated in neurons. It is now known that neurons have distinct classes of self-destruct programme that are spatially compartmentalised. In addition to the well-described intracellular suicide machinery in the neuronal soma, responsible for apoptosis, there is another, molecularly distinct, self-destruct programme localised in the axon. Evidence also supports the existence of compartmentalised degeneration programmes in synapses and dendrites. RGCs are no exception to this. Recent data, from in vitro studies and from an inherited mouse model of glaucoma, suggest that molecularly distinct degenerative pathways underlie the destruction of RGC somata and RGC axons. In various neurodegenerative diseases, axons, dendrites and synapses often degenerate well before the cells die, and there is increasing evidence that this is important for the production of clinical symptoms and signs. We hypothesise that such compartmentalised and autonomous programmes are of critical importance in the pathophysiology of glaucoma, and we suggest that studies of these processes are essential for a complete understanding of this complex disease.}, address = {Divisions of Pathology \& Cell Biology, Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, UK. a.whitmore@ucl.ac.uk}, author = {Whitmore, A. V. and Libby, R. T. and John, S. W.}, citeulike-article-id = {1567272}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.preteyeres.2005.04.004}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15953750}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15953750}, comment = {== uccessful inhibition of apoptosis alone is not sufficient for the treatment of glaucoma. == endritic self destruction is written about. Primate model of glaucoma demonstrated the earliest signs of pressure involved structural abnormailites of the dendritic arbour of RGCs. (and there are references - Watts, 2003, Fiala, 2002, Morgan, 2002, Weber, 1998, Shou, 2003) == he fact that dendritic dysfunction and degeneration often precede detectable cell body dysfunction, supports the hypothesis that a selective dendritic self-destruct mechanism analogous to but distinct from apoptosis, exists. == he site of initial injury in glaucoma is the axon where it is vulnerable as it apsses through the pores of the lamina cribrosa at the optic head. == paragraph about UPS involvenment in axonal degeneration. == ditto calcium. == ditto mitochondria == isual function may be compromised prior to cell loss. This may explain the poor correlation between visual function and RGC number in the early stages of experimental glaucoma (Harwertg et al 2002, Swanson et al, 2004).}, doi = {10.1016/j.preteyeres.2005.04.004}, issn = {1350-9462}, journal = {Prog Retin Eye Res}, keywords = {compartmental, neurodegeneration, rgc}, month = {November}, number = {6}, pages = {639--662}, posted-at = {2007-08-15 15:37:17}, priority = {5}, title = {Glaucoma: thinking in new ways-a r\^{o}le for autonomous axonal self-destruction and other compartmentalised processes?}, url = {http://dx.doi.org/10.1016/j.preteyeres.2005.04.004}, volume = {24}, year = {2005} }

TY - JOUR ID - citeulike:1567272 L3 - citeulike-article-id:1567272 N2 - Glaucoma is a common neurodegenerative disease that affects retinal ganglion cells (RGCs). Substantial effort is being expended to determine how RGCs die in glaucoma. As in other neurodegenerative diseases, the majority of effort focuses on characterising apoptotic self-destruct pathways. However, apoptosis is not the only self-destruct mechanism that may be activated in neurons. It is now known that neurons have distinct classes of self-destruct programme that are spatially compartmentalised. In addition to the well-described intracellular suicide machinery in the neuronal soma, responsible for apoptosis, there is another, molecularly distinct, self-destruct programme localised in the axon. Evidence also supports the existence of compartmentalised degeneration programmes in synapses and dendrites. RGCs are no exception to this. Recent data, from in vitro studies and from an inherited mouse model of glaucoma, suggest that molecularly distinct degenerative pathways underlie the destruction of RGC somata and RGC axons. In various neurodegenerative diseases, axons, dendrites and synapses often degenerate well before the cells die, and there is increasing evidence that this is important for the production of clinical symptoms and signs. We hypothesise that such compartmentalised and autonomous programmes are of critical importance in the pathophysiology of glaucoma, and we suggest that studies of these processes are essential for a complete understanding of this complex disease. IS - 6 JF - Prog Retin Eye Res SN - 1350-9462 AD - Divisions of Pathology & Cell Biology, Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, UK. a.whitmore@ucl.ac.uk EP - 662 TI - Glaucoma: thinking in new ways-a rôle for autonomous axonal self-destruction and other compartmentalised processes? VL - 24 SP - 639 KW - compartmental KW - neurodegeneration KW - rgc N1 - == uccessful inhibition of apoptosis alone is not sufficient for the treatment of glaucoma. == endritic self destruction is written about. Primate model of glaucoma demonstrated the earliest signs of pressure involved structural abnormailites of the dendritic arbour of RGCs. (and there are references - Watts, 2003, Fiala, 2002, Morgan, 2002, Weber, 1998, Shou, 2003) == he fact that dendritic dysfunction and degeneration often precede detectable cell body dysfunction, supports the hypothesis that a selective dendritic self-destruct mechanism analogous to but distinct from apoptosis, exists. == he site of initial injury in glaucoma is the axon where it is vulnerable as it apsses through the pores of the lamina cribrosa at the optic head. == paragraph about UPS involvenment in axonal degeneration. == ditto calcium. == ditto mitochondria == isual function may be compromised prior to cell loss. This may explain the poor correlation between visual function and RGC number in the early stages of experimental glaucoma (Harwertg et al 2002, Swanson et al, 2004). AU - Whitmore, AV AU - Libby, RT AU - John, SW PY - 2005/11// UR - http://dx.doi.org/10.1016/j.preteyeres.2005.04.004 ER -