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Necroptosis and Its Interactions wit...

D'Onofrio, Philippe Matteo.

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Necroptosis and Its Interactions with Focal Adhesion Kinase (FAK) and Extracellular Receptor Kinase (ERK1/2) Following Optic Nerve Injury.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Necroptosis and Its Interactions with Focal Adhesion Kinase (FAK) and Extracellular Receptor Kinase (ERK1/2) Following Optic Nerve Injury./
Author:	D'Onofrio, Philippe Matteo.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
Description:	300 p.
Notes:	Source: Dissertations Abstracts International, Volume: 81-06, Section: B.
Contained By:	Dissertations Abstracts International81-06B.
Subject:	Neurosciences. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27539540
ISBN:	9781392766309

Necroptosis and Its Interactions with Focal Adhesion Kinase (FAK) and Extracellular Receptor Kinase (ERK1/2) Following Optic Nerve Injury.
D'Onofrio, Philippe Matteo.

Necroptosis and Its Interactions with Focal Adhesion Kinase (FAK) and Extracellular Receptor Kinase (ERK1/2) Following Optic Nerve Injury. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 300 p.

Source: Dissertations Abstracts International, Volume: 81-06, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2019.

This item must not be sold to any third party vendors.

Glaucoma is the most prominent blinding disease in the world. It is irreversible and due to itsslow progression, patients often do not notice their decreased visual field until it is too late andthe damage is irreversible. Retinal ganglion cells are an essential step in the visual pathwayconnecting retinal photoreceptors to their targets in the brain, and they are the predominant celltypeaffected by glaucomatous degeneration. Although glaucoma has traditionally beenassociated with increased intraocular pressure, treatments designed to affect it have met withlimited success. This has led to a greater recognition of the importance of intracellular deathinducingmechanisms in the disease. Due to the protracted nature of neuron death in glaucoma,apoptosis has been regarded as the disease's primary, and therefore most studied, causativemechanism. However, recent advances have uncovered many more regulated neuron deathmechanisms, of which necroptosis is a prominent member. Necroptosis activation has beendetected in other central nervous system conditions, such as multiple sclerosis, Alzheimer'sdisease, and Parkinson's disease, as well as following ischemia in the brain and retina. The goalof this thesis is to examine the activation and role of necroptosis in the retina following optic nerve damage, a commonly used injury model to study glaucomatous neuron death. Some of thefactors associated with necroptosis have also been associated with cell-survival mechanisms,possibly contributing to aberrant cell-cycle re-entry. Therefore, the interplay between necroptosisand some prominent survival-inducing peptides is also examined. The goal `of this research is toprovide a basis for future work addressing neurodegeneration as a result of glaucoma or otherneurodegenerative disease.

ISBN: 9781392766309Subjects--Topical Terms:

588700
Neurosciences.
Subjects--Index Terms:

Extracellular Receptor Kinase 1/2

Necroptosis and Its Interactions with Focal Adhesion Kinase (FAK) and Extracellular Receptor Kinase (ERK1/2) Following Optic Nerve Injury.
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520 $a Glaucoma is the most prominent blinding disease in the world. It is irreversible and due to itsslow progression, patients often do not notice their decreased visual field until it is too late andthe damage is irreversible. Retinal ganglion cells are an essential step in the visual pathwayconnecting retinal photoreceptors to their targets in the brain, and they are the predominant celltypeaffected by glaucomatous degeneration. Although glaucoma has traditionally beenassociated with increased intraocular pressure, treatments designed to affect it have met withlimited success. This has led to a greater recognition of the importance of intracellular deathinducingmechanisms in the disease. Due to the protracted nature of neuron death in glaucoma,apoptosis has been regarded as the disease's primary, and therefore most studied, causativemechanism. However, recent advances have uncovered many more regulated neuron deathmechanisms, of which necroptosis is a prominent member. Necroptosis activation has beendetected in other central nervous system conditions, such as multiple sclerosis, Alzheimer'sdisease, and Parkinson's disease, as well as following ischemia in the brain and retina. The goalof this thesis is to examine the activation and role of necroptosis in the retina following optic nerve damage, a commonly used injury model to study glaucomatous neuron death. Some of thefactors associated with necroptosis have also been associated with cell-survival mechanisms,possibly contributing to aberrant cell-cycle re-entry. Therefore, the interplay between necroptosisand some prominent survival-inducing peptides is also examined. The goal `of this research is toprovide a basis for future work addressing neurodegeneration as a result of glaucoma or otherneurodegenerative disease.
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