Automated Nucleic Acid Purification for Large Samples

O'Brien, Darin P.

doi:10.1016/s1535-5535(04)00131-5

Cited by 3 publications

(3 citation statements)

References 5 publications

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“…APOE genotype was determined using a polymerase chain reaction method. DNA was isolated with Gentra Systems Autopure LS for Large Sample Nucleic Acid Purification [19]. We excluded 31 ε4- participants who had a family history (FH) of AD to isolate APOE as the primary AD genetic risk factor.…”

Section: Methodsmentioning

confidence: 99%

Five-Year Longitudinal Brain Volume Change in Healthy Elders at Genetic Risk for Alzheimer’s Disease

Reiter

Nielson

Durgerian

et al. 2016

JAD

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Neuropathological changes associated with Alzheimer’s disease (AD) precede symptom onset by more than a decade. Possession of an Apolipoprotein-E (APOE) ε4 allele is the strongest genetic risk factor for late onset AD. Cross-sectional studies of cognitively intact elders have noted smaller hippocampal/medial temporal volumes in ε4 carriers (ε4+) compared to ε4 non-carriers (ε4-). Few studies, however, have examined long-term, longitudinal, anatomical brain changes comparing healthy ε4+ and ε4- individuals. The current five-year study examined global and regional volumes of cortical and subcortical grey and white matter and ventricular size in 42 ε4+ and 30 ε4- individuals. Cognitively intact participants, ages 65-85 at study entry, underwent repeat anatomical MRI scans on three occasions: baseline, 1.5, and 4.75 years. Results indicated no between group volumetric differences at baseline. Over the follow-up interval, the ε4+ group experienced a greater rate of volume loss in total grey matter, bilateral hippocampi, right hippocampal subfields, bilateral lingual gyri, parahippocampal gyrus, and right lateral orbitofrontal cortex compared to the ε4- group. Greater loss in grey matter volumes in ε4+ participants were accompanied by greater increases in lateral, third and fourth ventricular volumes. Rate of change in white matter volumes did not differentiate the groups. The current results indicate that longitudinal measurements of brain atrophy can serve as a sensitive biomarker for identifying neuropathological changes in persons at genetic risk for AD and potentially, for assessing the efficacy of treatments designed to slow or prevent disease progression during the preclinical stage of AD.

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Section: Methodsmentioning

confidence: 99%

Five-Year Longitudinal Brain Volume Change in Healthy Elders at Genetic Risk for Alzheimer’s Disease

Reiter

Nielson

Durgerian

et al. 2016

JAD

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“…APOE genotype was determined using a polymerase chain reaction method. DNA was isolated with Gentra Systems Autopure LS for Large Sample Nucleic Acid Purification (O’Brien et al, 2001). Of the 109 enrolled participants, we excluded 31 participants with a family history of AD but without an APOE ε4 allele.…”

Section: Methodsmentioning

confidence: 99%

Genetic risk for Alzheimer's disease alters the five-year trajectory of semantic memory activation in cognitively intact elders

et al. 2015

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Healthy aging is associated with cognitive declines typically accompanied by increased task-related brain activity in comparison to younger counterparts. The Scaffolding Theory of Aging and Cognition (STAC) (Park and Reuter-Lorenz, 2009; Reuter-Lorenz and Park, 2014) posits that compensatory brain processes are responsible for maintaining normal cognitive performance in older adults, despite accumulation of aging-related neural damage. Cross-sectional studies indicate that cognitively intact elders at genetic risk for Alzheimer’s disease (AD) demonstrate patterns of increased brain activity compared to low risk elders, suggesting that compensation represents an early response to AD-associated pathology. Whether this compensatory response persists or declines with the onset of cognitive impairment can only be addressed using a longitudinal design. The current prospective, 5-year longitudinal study examined brain activation in APOE ε4 carriers (N=24) and non-carriers (N=21). All participants, ages 65–85 and cognitively intact at study entry, underwent task-activated fMRI, structural MRI, and neuropsychological assessments at baseline, 18, and 57 months. fMRI activation was measured in response to a semantic memory task requiring participants to discriminate famous from non-famous names. Results indicated that the trajectory of change in brain activation while performing this semantic memory task differed between APOE ε4 carriers and non-carriers. The APOE ε4 group exhibited greater activation than the Low Risk group at baseline, but they subsequently showed a progressive decline in activation during the follow-up periods with corresponding emergence of episodic memory loss and hippocampal atrophy. In contrast, the non-carriers demonstrated a gradual increase in activation over the 5-year period. Our results are consistent with the STAC model by demonstrating that compensation varies with the severity of underlying neural damage and can be exhausted with the onset of cognitive symptoms and increased structural brain pathology. Our fMRI results could not be attributed to changes in task performance, group differences in cerebral perfusion, or regional cortical atrophy.

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“…Deoxyribonucleic acid was isolated with the Gentra Systems Autopure LS for Large Sample Nucleic Acid Purification (O’Brien, Campbell, Morken, Bair, & Heath, 2001). The APOE-ε4 negative group included participants with ε23 ( n = 10) or ε33 ( n = 55) genotype; the APOE-ε4 positive group included participants with ε24 ( n = 2), ε34 ( n = 37), or ε44 ( n = 2) genotype.…”

Section: Methodsmentioning

confidence: 99%

Motor timing intraindividual variability in amnestic mild cognitive impairment and cognitively intact elders at genetic risk for Alzheimer’s disease

Kay

Seidenberg

Durgerian

et al. 2017

Journal of Clinical and Experimental Neuropsychology

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Introduction Intraindividual variability (IIV) in motor performance has been shown to predict future cognitive decline. The apolipoprotein E-epsilon 4 (APOE-ε4) allele is also a well-established risk factor for memory decline. Here, we present novel findings examining the influence of the APOE-ε4 allele on the performance of asymptomatic healthy elders in comparison to individuals with amnestic MCI (aMCI) on a fine motor synchronization, paced finger-tapping task (PFTT). Method Two Alzheimer’s disease (AD) risk groups, individuals with aMCI (n = 24) and cognitively intact APOE-ε4 carriers (n = 41), and a control group consisting of cognitively intact APOE-ε4 non-carriers (n = 65), completed the Rey Auditory Verbal Learning Test and the PFTT, which requires index finger tapping in synchrony with a visual stimulus (inter-stimulus interval = 333 milliseconds). Results Motor timing IIV, as reflected by the standard deviation of the inter-tap interval (ITI), was greater in the aMCI group relative to the two groups of cognitively intact elders; in contrast, all three groups had statistically equivalent mean ITI. No significant IIV differences were observed between the asymptomatic APOE-ε4 carriers and non-carriers. Poorer episodic memory performance was associated with greater IIV, particularly in the aMCI group. Conclusions Results suggest that increased IIV on a fine motor synchronization task is apparent in aMCI. This IIV measure was not sensitive in discriminating older asymptomatic individuals at genetic risk for AD from those without such a genetic risk. In contrast, episodic memory performance, a well-established predictor of cognitive decline in preclinical AD, was able to distinguish between the two cognitively intact groups based on genetic risk.

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Automated Nucleic Acid Purification for Large Samples

Cited by 3 publications

References 5 publications

Five-Year Longitudinal Brain Volume Change in Healthy Elders at Genetic Risk for Alzheimer’s Disease

Five-Year Longitudinal Brain Volume Change in Healthy Elders at Genetic Risk for Alzheimer’s Disease

Genetic risk for Alzheimer's disease alters the five-year trajectory of semantic memory activation in cognitively intact elders

Motor timing intraindividual variability in amnestic mild cognitive impairment and cognitively intact elders at genetic risk for Alzheimer’s disease

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