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Investigating the Role of the Membra...

Oseid, Daniel E.,

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Investigating the Role of the Membrane & Cellular Stress in Neurodegenerative Disorders /

Record Type:	Electronic resources : Monograph/item
Title/Author:	Investigating the Role of the Membrane & Cellular Stress in Neurodegenerative Disorders // Daniel E Oseid.
Author:	Oseid, Daniel E.,
Description:	1 electronic resource (159 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 82-01, Section: B.
Contained By:	Dissertations Abstracts International82-01B.
Subject:	Neurosciences. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27742340
ISBN:	9798662416802

Investigating the Role of the Membrane & Cellular Stress in Neurodegenerative Disorders /
Oseid, Daniel E.,

Investigating the Role of the Membrane & Cellular Stress in Neurodegenerative Disorders /Daniel E Oseid. - 1 electronic resource (159 pages)

Source: Dissertations Abstracts International, Volume: 82-01, Section: B.

Alzheimer's Disease (AD) is rapidly becoming one of the most economically burdensome diseases in the United States, affecting one out of every nine individuals aged 65 and older. Halting or slowing the progression of Alzheimer's disease (AD) is currently impossible with the tools and therapeutics currently available and a major obstacle to progress in the development of more efficacious therapeutics lies in the fact that initial disease mechanisms in AD may precede symptoms by more than a decade.Recent evidence suggests that the onset of AD and related dementias may stem from early alterations to the lipid membrane in the brain of diseased individuals. The main objective of this research was to understand the importance of the membrane in neurodegenerative disorders, with a particular focus on further understanding the basic biology of the glucocorticoid receptor (GR) and tau protein, both key players in the neurodegenerative disease process. For this work, basic mammalian cell culture models and highly-sensitive imaging techniques were used to further our understanding of likely initial events in AD. Here, we report that changes to membrane fluidity broadly affect the basic biology of GR and tau. For GR, increases to membrane fluidity initiated translocation in the absence of steroid, a novel translocation mechanism not previously reported. For tau protein, membrane fluidity affected rapid cellular uptake in a cell-specific and cholesterol-dependent manner. This work sheds light on early processes that may eventually set off pathological cascades that lead to neurodegeneration. The results from this dissertation will help guide future therapeutic strategies to help combat Alzheimer's disease.

English

ISBN: 9798662416802Subjects--Topical Terms:

588700
Neurosciences.
Subjects--Index Terms:

Benzyl alcohol

Investigating the Role of the Membrane & Cellular Stress in Neurodegenerative Disorders /
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502 $b Ph.D. $c Tulane University $d 2019.
520 $a Alzheimer's Disease (AD) is rapidly becoming one of the most economically burdensome diseases in the United States, affecting one out of every nine individuals aged 65 and older. Halting or slowing the progression of Alzheimer's disease (AD) is currently impossible with the tools and therapeutics currently available and a major obstacle to progress in the development of more efficacious therapeutics lies in the fact that initial disease mechanisms in AD may precede symptoms by more than a decade.Recent evidence suggests that the onset of AD and related dementias may stem from early alterations to the lipid membrane in the brain of diseased individuals. The main objective of this research was to understand the importance of the membrane in neurodegenerative disorders, with a particular focus on further understanding the basic biology of the glucocorticoid receptor (GR) and tau protein, both key players in the neurodegenerative disease process. For this work, basic mammalian cell culture models and highly-sensitive imaging techniques were used to further our understanding of likely initial events in AD. Here, we report that changes to membrane fluidity broadly affect the basic biology of GR and tau. For GR, increases to membrane fluidity initiated translocation in the absence of steroid, a novel translocation mechanism not previously reported. For tau protein, membrane fluidity affected rapid cellular uptake in a cell-specific and cholesterol-dependent manner. This work sheds light on early processes that may eventually set off pathological cascades that lead to neurodegeneration. The results from this dissertation will help guide future therapeutic strategies to help combat Alzheimer's disease.
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