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Peripheral Metabolic Disruptions Dri...

Carroll, Caitlin M.

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Peripheral Metabolic Disruptions Drive Sleep Impairments: Implications for the Pathophysiology of Alzheimer's Disease.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Peripheral Metabolic Disruptions Drive Sleep Impairments: Implications for the Pathophysiology of Alzheimer's Disease./
作者:	Carroll, Caitlin M.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2023,
面頁冊數:	236 p.
附註:	Source: Dissertations Abstracts International, Volume: 84-07, Section: B.
Contained By:	Dissertations Abstracts International84-07B.
標題:	Nanoscience. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30240932
ISBN:	9798368468662

Peripheral Metabolic Disruptions Drive Sleep Impairments: Implications for the Pathophysiology of Alzheimer's Disease.
Carroll, Caitlin M.

Peripheral Metabolic Disruptions Drive Sleep Impairments: Implications for the Pathophysiology of Alzheimer's Disease. - Ann Arbor : ProQuest Dissertations & Theses, 2023 - 236 p.

Source: Dissertations Abstracts International, Volume: 84-07, Section: B.

Thesis (Ph.D.)--Wake Forest University, 2023.

.

With no FDA-approved disease modifying treatments available, and an aging general population, Alzheimer's disease (AD) is a growing public health crisis. Individuals with type 2 diabetes (T2D), a disease also associated with aging, have an increased risk of AD. Despite the rising prevalence of both disease, the underlying mechanisms connecting their pathophysiology is unknown. The chapters in this dissertation consider sleep as a link between glucose dysregulation and amyloid-{CE}{ostrok} pathology. Specifically, we use acute modulation of peripheral glucose to understand the impacts on cerebral metabolism and neuronal activity, which can ultimately alter sleep. We also evaluate the independent impacts of age and A{CE}{ostrok} pathology on peripheral and cerebral glucose homeostasis. Further, we used a high fat, high sugar diet and metformin treatment to bidirectionally modulate peripheral glucose levels and alter sleep independent of changes in pathology. First, we established a metabolic signature of sleep-wake that is defined by a conserved, temporal relationship between ISF glucose and lactate. We then demonstrated this relationship is disrupted by acute hyper and hypoglycemia (Chapter 2). Next, we showed peripheral glucose dysregulation, as caused by HFD/HSW or A{CE}{ostrok} pathology, is sufficient to disrupt diurnal rhythms of cerebral metabolism and neuronal activity (Chapters 3-4). Ultimately, this leads to impaired slow wave sleep. Finally, we demonstrated rescuing peripheral glucose homeostasis with metformin treatment can normalize diurnal rhythms and slow wave sleep (Chapter 4). Collectively, we identified a cyclic relationship between peripheral glucose homeostasis and sleep, both modifiable risk factors in the progression of AD. Moreover, we showed modulating peripheral glucose homeostasis directly impacts cerebral metabolism and neuronal activity, ultimately affecting slow wave sleep. This provides an explanation for the elevated risk of AD in individuals with T2D and highlights potential therapeutic targets for mitigating this risk.{A0}

ISBN: 9798368468662Subjects--Topical Terms:

587832
Nanoscience.
Subjects--Index Terms:

Sleep impairments

Peripheral Metabolic Disruptions Drive Sleep Impairments: Implications for the Pathophysiology of Alzheimer's Disease.
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520 $a With no FDA-approved disease modifying treatments available, and an aging general population, Alzheimer's disease (AD) is a growing public health crisis. Individuals with type 2 diabetes (T2D), a disease also associated with aging, have an increased risk of AD. Despite the rising prevalence of both disease, the underlying mechanisms connecting their pathophysiology is unknown. The chapters in this dissertation consider sleep as a link between glucose dysregulation and amyloid-{CE}{ostrok} pathology. Specifically, we use acute modulation of peripheral glucose to understand the impacts on cerebral metabolism and neuronal activity, which can ultimately alter sleep. We also evaluate the independent impacts of age and A{CE}{ostrok} pathology on peripheral and cerebral glucose homeostasis. Further, we used a high fat, high sugar diet and metformin treatment to bidirectionally modulate peripheral glucose levels and alter sleep independent of changes in pathology. First, we established a metabolic signature of sleep-wake that is defined by a conserved, temporal relationship between ISF glucose and lactate. We then demonstrated this relationship is disrupted by acute hyper and hypoglycemia (Chapter 2). Next, we showed peripheral glucose dysregulation, as caused by HFD/HSW or A{CE}{ostrok} pathology, is sufficient to disrupt diurnal rhythms of cerebral metabolism and neuronal activity (Chapters 3-4). Ultimately, this leads to impaired slow wave sleep. Finally, we demonstrated rescuing peripheral glucose homeostasis with metformin treatment can normalize diurnal rhythms and slow wave sleep (Chapter 4). Collectively, we identified a cyclic relationship between peripheral glucose homeostasis and sleep, both modifiable risk factors in the progression of AD. Moreover, we showed modulating peripheral glucose homeostasis directly impacts cerebral metabolism and neuronal activity, ultimately affecting slow wave sleep. This provides an explanation for the elevated risk of AD in individuals with T2D and highlights potential therapeutic targets for mitigating this risk.{A0}
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