Cell death in age-related macular degeneration.

R. Adler, C. Curcio, D. Hicks, D. Price, F. Wong

Research output: Contribution to journalArticle

Abstract

The cellular and molecular mechanisms underlying the death of photoreceptors and other retinal cells in age-related macular degeneration (AMD) remain poorly understood. Some of the questions for which answers need to be sought, and which are explicitly or implicitly addressed in this article include: (1) how do patterns of cell death in AMD compare, qualitatively and quantitatively, with "normal" cell death in aging retinas, and with cell death in retinitis pigmentosa (RP) and its animal models; (2) is apoptosis involved in AMD; (3) is there any evidence that rods are necessary for cone survival; (4) if the answer is yes, is there evidence that rods produce one or more survival-promoting factor(s) that act directly on cones; (5) are the effects of rods upon cones exclusively mediated by diffusible factors, or do they also involve contact-mediated interactions; (6) is there any evidence that photoreceptors regulate the survival and/or function of RPE and Müller cells, as well as the interactions between these cells and cones; (7) are trophic factors and their receptors in the macula different from those in other parts of the retina; and (8) are toxic mechanisms involved in the onset and progression of cell death in AMD? Clear cut answers to most of these (and related) questions about cell death in AMD are not yet available. The goal of this article is to summarize discussion that should help in the formulation of suitable hypotheses, amenable to experimental analysis. To provide a platform for such discussion, we present an overview of progress made in recent years in the analysis of other retinal degenerations and of neuronal degenerations in other regions of the CNS. We conclude with an overview of concepts and speculation derived from our current research.

Original languageEnglish (US)
Pages (from-to)31
Number of pages1
JournalMolecular Vision
Volume5
StatePublished - Nov 3 1999

Fingerprint

Macular Degeneration
Cell Death
Vertebrate Photoreceptor Cells
Retina
Retinal Degeneration
Retinitis Pigmentosa
Growth Factor Receptors
Poisons
Cell Communication
Animal Models
Apoptosis
Research

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Adler, R., Curcio, C., Hicks, D., Price, D., & Wong, F. (1999). Cell death in age-related macular degeneration. Molecular Vision, 5, 31.

Cell death in age-related macular degeneration. / Adler, R.; Curcio, C.; Hicks, D.; Price, D.; Wong, F.

In: Molecular Vision, Vol. 5, 03.11.1999, p. 31.

Research output: Contribution to journalArticle

Adler, R, Curcio, C, Hicks, D, Price, D & Wong, F 1999, 'Cell death in age-related macular degeneration.', Molecular Vision, vol. 5, pp. 31.
Adler R, Curcio C, Hicks D, Price D, Wong F. Cell death in age-related macular degeneration. Molecular Vision. 1999 Nov 3;5:31.
Adler, R. ; Curcio, C. ; Hicks, D. ; Price, D. ; Wong, F. / Cell death in age-related macular degeneration. In: Molecular Vision. 1999 ; Vol. 5. pp. 31.
@article{1de217421f9f414fa2f8a05e3eb4829b,
title = "Cell death in age-related macular degeneration.",
abstract = "The cellular and molecular mechanisms underlying the death of photoreceptors and other retinal cells in age-related macular degeneration (AMD) remain poorly understood. Some of the questions for which answers need to be sought, and which are explicitly or implicitly addressed in this article include: (1) how do patterns of cell death in AMD compare, qualitatively and quantitatively, with {"}normal{"} cell death in aging retinas, and with cell death in retinitis pigmentosa (RP) and its animal models; (2) is apoptosis involved in AMD; (3) is there any evidence that rods are necessary for cone survival; (4) if the answer is yes, is there evidence that rods produce one or more survival-promoting factor(s) that act directly on cones; (5) are the effects of rods upon cones exclusively mediated by diffusible factors, or do they also involve contact-mediated interactions; (6) is there any evidence that photoreceptors regulate the survival and/or function of RPE and M{\"u}ller cells, as well as the interactions between these cells and cones; (7) are trophic factors and their receptors in the macula different from those in other parts of the retina; and (8) are toxic mechanisms involved in the onset and progression of cell death in AMD? Clear cut answers to most of these (and related) questions about cell death in AMD are not yet available. The goal of this article is to summarize discussion that should help in the formulation of suitable hypotheses, amenable to experimental analysis. To provide a platform for such discussion, we present an overview of progress made in recent years in the analysis of other retinal degenerations and of neuronal degenerations in other regions of the CNS. We conclude with an overview of concepts and speculation derived from our current research.",
author = "R. Adler and C. Curcio and D. Hicks and D. Price and F. Wong",
year = "1999",
month = "11",
day = "3",
language = "English (US)",
volume = "5",
pages = "31",
journal = "Molecular Vision",
issn = "1090-0535",

}

TY - JOUR

T1 - Cell death in age-related macular degeneration.

AU - Adler, R.

AU - Curcio, C.

AU - Hicks, D.

AU - Price, D.

AU - Wong, F.

PY - 1999/11/3

Y1 - 1999/11/3

N2 - The cellular and molecular mechanisms underlying the death of photoreceptors and other retinal cells in age-related macular degeneration (AMD) remain poorly understood. Some of the questions for which answers need to be sought, and which are explicitly or implicitly addressed in this article include: (1) how do patterns of cell death in AMD compare, qualitatively and quantitatively, with "normal" cell death in aging retinas, and with cell death in retinitis pigmentosa (RP) and its animal models; (2) is apoptosis involved in AMD; (3) is there any evidence that rods are necessary for cone survival; (4) if the answer is yes, is there evidence that rods produce one or more survival-promoting factor(s) that act directly on cones; (5) are the effects of rods upon cones exclusively mediated by diffusible factors, or do they also involve contact-mediated interactions; (6) is there any evidence that photoreceptors regulate the survival and/or function of RPE and Müller cells, as well as the interactions between these cells and cones; (7) are trophic factors and their receptors in the macula different from those in other parts of the retina; and (8) are toxic mechanisms involved in the onset and progression of cell death in AMD? Clear cut answers to most of these (and related) questions about cell death in AMD are not yet available. The goal of this article is to summarize discussion that should help in the formulation of suitable hypotheses, amenable to experimental analysis. To provide a platform for such discussion, we present an overview of progress made in recent years in the analysis of other retinal degenerations and of neuronal degenerations in other regions of the CNS. We conclude with an overview of concepts and speculation derived from our current research.

AB - The cellular and molecular mechanisms underlying the death of photoreceptors and other retinal cells in age-related macular degeneration (AMD) remain poorly understood. Some of the questions for which answers need to be sought, and which are explicitly or implicitly addressed in this article include: (1) how do patterns of cell death in AMD compare, qualitatively and quantitatively, with "normal" cell death in aging retinas, and with cell death in retinitis pigmentosa (RP) and its animal models; (2) is apoptosis involved in AMD; (3) is there any evidence that rods are necessary for cone survival; (4) if the answer is yes, is there evidence that rods produce one or more survival-promoting factor(s) that act directly on cones; (5) are the effects of rods upon cones exclusively mediated by diffusible factors, or do they also involve contact-mediated interactions; (6) is there any evidence that photoreceptors regulate the survival and/or function of RPE and Müller cells, as well as the interactions between these cells and cones; (7) are trophic factors and their receptors in the macula different from those in other parts of the retina; and (8) are toxic mechanisms involved in the onset and progression of cell death in AMD? Clear cut answers to most of these (and related) questions about cell death in AMD are not yet available. The goal of this article is to summarize discussion that should help in the formulation of suitable hypotheses, amenable to experimental analysis. To provide a platform for such discussion, we present an overview of progress made in recent years in the analysis of other retinal degenerations and of neuronal degenerations in other regions of the CNS. We conclude with an overview of concepts and speculation derived from our current research.

UR - http://www.scopus.com/inward/record.url?scp=0033520644&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033520644&partnerID=8YFLogxK

M3 - Article

VL - 5

SP - 31

JO - Molecular Vision

JF - Molecular Vision

SN - 1090-0535

ER -