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Tissue Damage Quantification in Alzh...
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Zhao, Yue.
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Tissue Damage Quantification in Alzheimer's Disease Brain via Magnetic Resonance Gradient Echo Plural Contrast Imaging (GEPCI).
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Tissue Damage Quantification in Alzheimer's Disease Brain via Magnetic Resonance Gradient Echo Plural Contrast Imaging (GEPCI)./
作者:
Zhao, Yue.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2017,
面頁冊數:
104 p.
附註:
Source: Dissertation Abstracts International, Volume: 78-09(E), Section: B.
Contained By:
Dissertation Abstracts International78-09B(E).
標題:
Biophysics. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10269174
ISBN:
9781369706499
Tissue Damage Quantification in Alzheimer's Disease Brain via Magnetic Resonance Gradient Echo Plural Contrast Imaging (GEPCI).
Zhao, Yue.
Tissue Damage Quantification in Alzheimer's Disease Brain via Magnetic Resonance Gradient Echo Plural Contrast Imaging (GEPCI).
- Ann Arbor : ProQuest Dissertations & Theses, 2017 - 104 p.
Source: Dissertation Abstracts International, Volume: 78-09(E), Section: B.
Thesis (Ph.D.)--Washington University in St. Louis, 2017.
Alzheimer's disease (AD) affected approximately 48 million people worldwide in 2015. Its devastating consequences have stimulated an intense search for AD prevention and treatment. Clinically, AD is characterized by memory deficits and progressive cognitive impairment, leading to dementia. Over the past two to three decades, researchers have found that amyloid-beta (Abeta) plaques and neurofibrillary tau tangles occur during a long pre-symptomatic period (preclinical stage) before the onset of clinical symptoms. As a result, identification of the preclinical stage is essential for the initiation of prevention trials in asymptomatic individuals. Currently, Positron Emission Tomography (PET) imaging with injected 11C or 18F containing radiotracers (e.g., Pittsburgh compound B, PiB or florbetapir-fluorine-18, 18F-AV-45) is widely used to detect amyloid deposition in vivo and to identify this preclinical stage. However, PET scans are time consuming (about 1 hour), require injection of a radiotracer, thus, exposing the patient to ionizing radiation. After the preclinical stage, AD patients begin to show clinical symptoms, referred as a very mild or mild AD group. Post-mortem studies show that neuronal damage is the most proximate pathological substrate of cognitive impairment in AD compared with amyloid and tau deposition. Thus, a diagnostic tool is needed for detection of neuronal loss in vivo. As a faster, non-invasive, and radiation free imaging technique, Magnetic Resonance Imaging (MRI) plays an important role in the diagnosis of cognitive diseases. Conventional MRI yields superb definition of brain anatomy and structure and provide important volumetric information (e.g., brain atrophy). However, conventional MRI cannot provide microstructural and functional insight into the pathology of AD.
ISBN: 9781369706499Subjects--Topical Terms:
518360
Biophysics.
Tissue Damage Quantification in Alzheimer's Disease Brain via Magnetic Resonance Gradient Echo Plural Contrast Imaging (GEPCI).
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Alzheimer's disease (AD) affected approximately 48 million people worldwide in 2015. Its devastating consequences have stimulated an intense search for AD prevention and treatment. Clinically, AD is characterized by memory deficits and progressive cognitive impairment, leading to dementia. Over the past two to three decades, researchers have found that amyloid-beta (Abeta) plaques and neurofibrillary tau tangles occur during a long pre-symptomatic period (preclinical stage) before the onset of clinical symptoms. As a result, identification of the preclinical stage is essential for the initiation of prevention trials in asymptomatic individuals. Currently, Positron Emission Tomography (PET) imaging with injected 11C or 18F containing radiotracers (e.g., Pittsburgh compound B, PiB or florbetapir-fluorine-18, 18F-AV-45) is widely used to detect amyloid deposition in vivo and to identify this preclinical stage. However, PET scans are time consuming (about 1 hour), require injection of a radiotracer, thus, exposing the patient to ionizing radiation. After the preclinical stage, AD patients begin to show clinical symptoms, referred as a very mild or mild AD group. Post-mortem studies show that neuronal damage is the most proximate pathological substrate of cognitive impairment in AD compared with amyloid and tau deposition. Thus, a diagnostic tool is needed for detection of neuronal loss in vivo. As a faster, non-invasive, and radiation free imaging technique, Magnetic Resonance Imaging (MRI) plays an important role in the diagnosis of cognitive diseases. Conventional MRI yields superb definition of brain anatomy and structure and provide important volumetric information (e.g., brain atrophy). However, conventional MRI cannot provide microstructural and functional insight into the pathology of AD.
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The approach developed in Yablonskiy's lab is based on the Gradient Echo Plural Contrast Imaging (GEPCI) protocol, which provides quantitative in vivo measurements of transverse relaxation properties of the tissue water 1H spins as determined from the gradient echo MRI signal. The measurements are corrected for macroscopic magnetic field inhomogeneity effects and physiologic-motion-driven fluctuations in magnetic field as these are the major artifacts present with the gradient echo technique. The principal relaxation property used in this dissertation is the tissue-specific transverse relaxation rate constant, R2*. The R2* value reflects the microscopic and mesoscopic magnetic field inhomogeneities rising from the complex tissue-water-environment within the human brain. In turn, changes in R2* reflect changes in the tissue's microscopic and mesoscopic tissue structure.
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GEPCI provides a new approach for evaluation of AD-related tissue pathology in vivo in the preclinical and early symptomatic stages of AD. Since MRI is widely available worldwide and does not require radiation exposure, it provides the opportunity to obtain new information on the pathogenesis of AD and for pre-screening cohorts (stratification) for clinical drug trials. (Abstract shortened by ProQuest.).
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