Magnetic Resonance Imaging Traits in Siblings Discordant for Alzheimer Disease

Cuenco, Karen T.; Green, Robert C; Zhang, J; Lunetta, Kathryn L.; Erlich, Porat M.; Cupples, L. Adrienne; Farrer, Lindsay A.; DeCarli, Charles

doi:10.1111/j.1552-6569.2007.00191.x

Cited by 25 publications

(21 citation statements)

References 56 publications

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“…The FSE pulse sequences used in the ADNI were not standardized between research sites, consistent with protocols of many other large scale studies including the Framingham Heart Study (DeCarli et al, 2005), MIRAGE (Cuenco et al, 2008), and many clinical drug trials.…”

Section: Discussionmentioning

confidence: 99%

Whole brain quantitative T2 MRI across multiple scanners with dual echo FSE: Applications to AD, MCI, and normal aging

2010

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The ability to pool data from multiple MRI scanners is becoming increasingly important with the influx in multi-site research studies. Fast spin echo (FSE) dual spin echo sequences are often chosen for such studies based principally on their short acquisition time and clinically useful contrasts they provide for assessing gross pathology. The practicality of measuring FSE-T2 relaxation properties has rarely been assessed. Here, FSE-T2 relaxation properties are examined across the three main scanner vendors (General Electric (GE), Philips, and Siemens). The American College of Radiology (ACR) phantom was scanned on four 1.5T platforms (two GE, one Philips, and one Siemens) to determine if the dual echo pulse sequence is susceptible to vendor-based variance. In addition, data from 85 subjects spanning the spectrum of normal aging, mild cognitive impairment (MCI), and Alzheimer's disease (AD) was obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) to affirm the presence of any phantom based between vendor variance and determine the relationship between this variance and disease. FSE-T2 relaxation properties, including peak FSE-T2 and histogram width, were calculated for each phantom and human subject. Direct correspondence was found between the phantom and human subject data. Peak FSE-T2 of Siemens scanners was consistently at least 20ms prolonged compared to GE and Philips. Siemens scanners showed broader FSE-T2 histograms than the other © 2010 Elsevier Inc. All rights reserved. * Corresponding Author: Ron Killiany, PhD, Boston University School of Medicine, 700 Albany Street, Room W-701, Boston, MA 02118, killiany@bu.eduPhone: 617-638-8082, Fax: 617-638-4922. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Data used in the preparation for this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (http://www.loni.ucla.edu/ADNI). As such, the investigator's within the ADNI contributed to the design and implementation of ADNI and/or provided data, but did not participate in analysis or writing of this manuscript. A complete listing of ADNI investigators can be found at www.loni.ucla.edu/ADNI/Collaboration/ADNI_Citation.shtml. Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by an insidious onset followed by gradual decline in cognitive function. It is the most common form of dementia and is quickly becoming a global crisis, affecting approximately 10% of individuals over age 65 and nearly 50% of individuals over 85 years of age (Evans et al., 1989). An additional 19% of individua...

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Section: Discussionmentioning

confidence: 99%

Whole brain quantitative T2 MRI across multiple scanners with dual echo FSE: Applications to AD, MCI, and normal aging

2010

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“…AD is the most common pathogenesis of age-related dementia, which is one of the leading causes of death for those aged 65 years and older [2]. It is a chronic and progressive neurodegenerative disorder characterized by degeneration and loss of neurons in the brain that usually begins with memory loss simultaneously [3]. Though the pathogenesis of AD is still unknown, it has been proved that accumulation of beta-amyloid (Aβ) fibrillar deposition in senile plaques and neurofibrillary tangles lesions in specific areas of brain correlates with the progression of cognitive dysfunction in AD patients [4,5,6].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Fucoidan on Aβ25–35 and d-Gal-Induced Neurotoxicity in PC12 Cells and d-Gal-Induced Cognitive Dysfunction in Mice

et al. 2017

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Alzheimer’s disease (AD) is a chronic neurodegenerative disease which contributes to memory loss and cognitive decline in the elderly. Fucoidan, extracted from brown algae, is a complex sulfated polysaccharide and potential bioactive compound. In this study, we investigated whether fucoidan protects PC12 cells from apoptosis induced by a combination of beta-amyloid 25–35 (Aβ25–35) and d-galactose (d-Gal), and improves learning and memory impairment in AD model mice. The results indicated that fucoidan could inhibit the release of cytochrome c from the mitochondria to cytosol and activation of caspases, and increase the expression of apoptosis inhibitor proteins (IAPs), including livin and X-linked IAP (XIAP) in PC12 cells damaged by Aβ25–35 and d-Gal-induction. Fucoidan reversed the decreased activity of acetylcholine (ACh) and choline acetyl transferase (ChAT), as well as the increased activity of acetylcholine esterase (AChE), in AD model mice induced by infusion of d-Gal. Furthermore, fucoidan improved antioxidant activity in vitro and in vivo by activation of superoxide dismutase (SOD) and glutathione (GSH). These results suggested that fucoidan could protect PC12 cells from apoptosis and ameliorate the learning and memory impairment in AD model mice, which appeared to be due to regulating the cholinergic system, reducing oxidative stress, and inhibiting the caspase-dependent apoptosis pathway.

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“…Hippocampal atrophy is well known to occur early in the disease and is correlated with impaired memory function as well as pathology (Deweer et al, 1995; Nagy et al, 1996). Previously, we demonstrated in this sample of families that hippocampal atrophy is highly heritable (Lunetta et al, 2007) and may be a marker of subclinical disease (T. Cuenco et al, 2008a).…”

Section: Discussionmentioning

confidence: 88%

“…A detailed description of the MIRAGE magnetic resonance imaging (MRI) methods and traits has been published elsewhere (T.Cuenco et al, 2008a; 2008b). Briefly, beginning in 2002 MRIs were obtained from subjects using 1.5 Tesla magnetic field strength scanners.…”

Section: Methodsmentioning

confidence: 99%

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Association of TTR polymorphisms with hippocampal atrophy in Alzheimer disease families

Cuenco

Friedland

Baldwin

et al. 2011

Neurobiology of Aging

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In vitro and animal model studies suggest that transthyretin (TTR) inhibits the production of the amyloid β protein, a major contributor to Alzheimer disease (AD) pathogenesis. We evaluated the association of 16 TTR single nucleotide polymorphisms (SNPs) with AD risk in 158 African American and 469 Caucasian discordant sibships from the MIRAGE Study. There was no evidence for association of TTR with AD in either population sample. To examine the possibility that TTR SNPs affect specific components of the AD process, we tested association of these SNPs with four measures of neurodegeneration and cerebrovascular disease defined by magnetic Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

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Magnetic Resonance Imaging Traits in Siblings Discordant for Alzheimer Disease

Cited by 25 publications

References 56 publications

Whole brain quantitative T2 MRI across multiple scanners with dual echo FSE: Applications to AD, MCI, and normal aging

Whole brain quantitative T2 MRI across multiple scanners with dual echo FSE: Applications to AD, MCI, and normal aging

Protective Effects of Fucoidan on Aβ25–35 and d-Gal-Induced Neurotoxicity in PC12 Cells and d-Gal-Induced Cognitive Dysfunction in Mice

Association of TTR polymorphisms with hippocampal atrophy in Alzheimer disease families

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