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class="o-input__droplist1"><label for="c-sort1">Sort By:</label><select name="sort" id="c-sort1" form="facetForm"><option selected="" value="rel">Relevance</option><option value="a-title">A-Z By Title</option><option value="z-title">Z-A By Title</option><option value="a-author">A-Z By Author</option><option value="z-author">Z-A By Author</option><option value="asc">Date Ascending</option><option value="desc">Date Descending</option></select></div><div class="o-input__droplist1 c-sort__page-input"><label for="c-sort2">Show:</label><select name="rows" id="c-sort2" form="facetForm"><option selected="" value="10">10</option><option value="20">20</option><option value="30">30</option><option value="40">40</option><option value="50">50</option><option value="100">100</option></select></div></div><input type="hidden" name="start" form="facetForm" value="0"/><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" class="c-pagination__item">4</a></li><li><a href="" aria-label="go to result set 24" class="c-pagination__item">24</a></li><li class="c-pagination__next"><a href="" aria-label="go to Next result set">Next</a></li></ul></nav></div><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/12v4b2m7"><div class="c-clientmarkup">Amyloid biomarkers: pushing the limits of early detection</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2016)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">This scientific commentary refers to ‘Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography’, by Palmqvist et al. (doi: 10.1093/brain/aww015 ).</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/12v4b2m7"><img src="/cms-assets/d1fda7de14fdd37565efdf6e1e8f65d508a283ddd36ba45579870affceba1541" alt="Cover page: Amyloid biomarkers: pushing the limits of early detection"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/7dp8c6v1"><div class="c-clientmarkup">Late-onset Alzheimer Disease.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2019)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Purpose of review</h3>Alzheimer disease (AD) is the most common cause of late-onset dementia. This article describes the epidemiology, genetic and environmental risk factors, clinical diagnosis, biomarkers, and treatment of late-onset AD, defined by age of onset of 65 years or older.<h3>Recent findings</h3>An estimated 5.7 million Americans are living with AD dementia, with the number of affected individuals growing rapidly because of an aging population. Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease. The primary genetic risk factor for late-onset AD is the apolipoprotein E (APOE) ε4 allele. AD typically presents with early and prominent episodic memory loss, although this clinical syndrome is neither sensitive nor specific for underlying AD neuropathology. Emerging CSF and imaging biomarkers can now detect the key neuropathologic features of the disease (amyloid plaques, neurofibrillary tangles, and neurodegeneration) in living people, allowing for characterization of patients based on biological measures. A comprehensive treatment plan for AD includes use of symptomatic medications, optimal treatment of comorbid conditions and neuropsychiatric symptoms, counseling about safety and future planning, and referrals to community resources.<h3>Summary</h3>AD is very common in older neurologic patients. Neurologists should set the standard for the diagnosis and care of patients with AD and should be familiar with emerging biomarkers that have transformed AD research and are primed to enter the clinical arena.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/7dp8c6v1"><img src="/cms-assets/2b14d424d7e1dfec284712aa2cbbf1f39d687f471a1216d0a289a8ba563f4929" alt="Cover page: Late-onset Alzheimer Disease."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/4r41g6f8"><div class="c-clientmarkup">Amyloid imaging in the differential diagnosis of dementia: review and potential clinical applications</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ALaforce%2C%20Robert">Laforce, Robert</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2011)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">In the past decade, positron emission tomography (PET) with carbon-11-labeled Pittsburgh Compound B (PIB) has revolutionized the neuroimaging of aging and dementia by enabling in vivo detection of amyloid plaques, a core pathologic feature of Alzheimer's disease (AD). Studies suggest that PIB-PET is sensitive for AD pathology, can distinguish AD from non-AD dementia (for example, frontotemporal lobar degeneration), and can help determine whether mild cognitive impairment is due to AD. Although the short half-life of the carbon-11 radiolabel has thus far limited the use of PIB to research, a second generation of tracers labeled with fluorine-18 has made it possible for amyloid PET to enter the clinical era. In the present review, we summarize the literature on amyloid imaging in a range of neurodegenerative conditions. We focus on potential clinical applications of amyloid PET and its role in the differential diagnosis of dementia. We suggest that amyloid imaging will be particularly useful in the evaluation of mildly affected, clinically atypical or early age-at-onset patients, and illustrate this with case vignettes from our practice. We emphasize that amyloid imaging should supplement (not replace) a detailed clinical evaluation. We caution against screening asymptomatic individuals, and discuss the limited positive predictive value in older populations. Finally, we review limitations and unresolved questions related to this exciting new technique.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/4r41g6f8"><img src="/cms-assets/a4a8582d74842eb9192148646eef9cde37b0085ac04bad286c23ca16bd661dc7" alt="Cover page: Amyloid imaging in the differential diagnosis of dementia: review and potential clinical applications"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/6wq5r1p8"><div class="c-clientmarkup">Identifying degenerative effects of repetitive head trauma with neuroimaging: a clinically-oriented review</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AAsken%2C%20Breton%20M">Asken, Breton M</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2021)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background and scope of review</h3>Varying severities and frequencies of head trauma may result in dynamic acute and chronic pathophysiologic responses in the brain. Heightened attention to long-term effects of head trauma, particularly repetitive head trauma, has sparked recent efforts to identify neuroimaging biomarkers of underlying disease processes. Imaging modalities like structural magnetic resonance imaging (MRI) and positron emission tomography (PET) are the most clinically applicable given their use in neurodegenerative disease diagnosis and differentiation. In recent years, researchers have targeted repetitive head trauma cohorts in hopes of identifying in vivo biomarkers for underlying biologic changes that might ultimately improve diagnosis of chronic traumatic encephalopathy (CTE) in living persons. These populations most often include collision sport athletes (e.g., American football, boxing) and military veterans with repetitive low-level blast exposure. We provide a clinically-oriented review of neuroimaging data from repetitive head trauma cohorts based on structural MRI, FDG-PET, Aβ-PET, and tau-PET. We supplement the review with two patient reports of neuropathology-confirmed, clinically impaired adults with prior repetitive head trauma who underwent structural MRI, FDG-PET, Aβ-PET, and tau-PET in addition to comprehensive clinical examinations before death.<h3>Review conclusions</h3>Group-level comparisons to controls without known head trauma have revealed inconsistent regional volume differences, with possible propensity for medial temporal, limbic, and subcortical (thalamus, corpus callosum) structures. Greater frequency and severity (i.e., length) of cavum septum pellucidum (CSP) is observed in repetitive head trauma cohorts compared to unexposed controls. It remains unclear whether CSP predicts a particular neurodegenerative process, but CSP presence should increase suspicion that clinical impairment is at least partly attributable to the individual's head trauma exposure (regardless of underlying disease). PET imaging similarly has not revealed a prototypical metabolic or molecular pattern associated with repetitive head trauma or predictive of CTE based on the most widely studied radiotracers. Given the range of clinical syndromes and neurodegenerative pathologies observed in a subset of adults with prior repetitive head trauma, structural MRI and PET imaging may still be useful for differential diagnosis (e.g., assessing suspected Alzheimer's disease).</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/6wq5r1p8"><img src="/cms-assets/a425a32114cd6416bd5582c47b5fade3a5b06e877698f322f9c43b549179e045" alt="Cover page: Identifying degenerative effects of repetitive head trauma with neuroimaging: a clinically-oriented review"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2t12b939"><div class="c-clientmarkup">The Role of Amyloid PET in Imaging Neurodegenerative Disorders: A Review.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AChapleau%2C%20Marianne">Chapleau, Marianne</a>; </li><li><a href="/search/?q=author%3AIaccarino%2C%20Leonardo">Iaccarino, Leonardo</a>; </li><li><a href="/search/?q=author%3ASoleimani-Meigooni%2C%20David">Soleimani-Meigooni, David</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2022)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Imaging of amyloid deposition using PET has been available in research studies for 2 decades and has been approved for clinical use by the U.S. Food and Drug Administration, the European Medicines Agency, and other regulatory agencies around the world. Amyloid PET is a crucial tool for the diagnosis of Alzheimer disease, as it allows the noninvasive detection of amyloid plaques, a core neuropathologic feature that defines the disease. The clinical use of amyloid PET is expected to increase with recent accelerated approval in the United States of aducanumab, an antiamyloid monoclonal antibody, for the treatment of mild cognitive impairment and mild dementia due to Alzheimer disease. However, amyloid pathology can also be found in cognitively unimpaired older adults and in patients with other neurodegenerative disorders. The aim of this review is to provide an up-to-date overview of the application of amyloid PET in neurodegenerative diseases. We provide an in-depth analysis of the clinical, pathologic, and imaging correlates; a comparison with other available biomarkers; and a review of the application of amyloid PET in clinical trials and clinical utility studies.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/534865f3"><div class="c-clientmarkup">The Rise of Pseudomedicine for Dementia and Brain Health</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AHellmuth%2C%20Joanna">Hellmuth, Joanna</a>; </li><li><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMiller%2C%20Bruce%20L">Miller, Bruce L</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2019)</div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/00r0j5xb"><div class="c-clientmarkup">Executive Dysfunction</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a>; </li><li><a href="/search/?q=author%3AStephens%2C%20Melanie%20L">Stephens, Melanie L</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3APossin%2C%20Katherine%20L">Possin, Katherine L</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2015)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Purpose of review</h3>Executive functions represent a constellation of cognitive abilities that drive goal-oriented behavior and are critical to the ability to adapt to an ever-changing world. This article provides a clinically oriented approach to classifying, localizing, diagnosing, and treating disorders of executive function, which are pervasive in clinical practice.<h3>Recent findings</h3>Executive functions can be split into four distinct components: working memory, inhibition, set shifting, and fluency. These components may be differentially affected in individual patients and act together to guide higher-order cognitive constructs such as planning and organization. Specific bedside and neuropsychological tests can be applied to evaluate components of executive function. While dysexecutive syndromes were first described in patients with frontal lesions, intact executive functioning relies on distributed neural networks that include not only the prefrontal cortex, but also the parietal cortex, basal ganglia, thalamus, and cerebellum. Executive dysfunction arises from injury to any of these regions, their white matter connections, or neurotransmitter systems. Dysexecutive symptoms therefore occur in most neurodegenerative diseases and in many other neurologic, psychiatric, and systemic illnesses. Management approaches are patient specific and should focus on treatment of the underlying cause in parallel with maximizing patient function and safety via occupational therapy and rehabilitation.<h3>Summary</h3>Executive dysfunction is extremely common in patients with neurologic disorders. Diagnosis and treatment hinge on familiarity with the clinical components and neuroanatomic correlates of these complex, high-order cognitive processes.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/00r0j5xb"><img src="/cms-assets/cfd51b0acfa8654a53e71c5672c257c094e9a74aa0748fb2301dee7309982fef" alt="Cover page: Executive Dysfunction"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/0099d4tn"><div class="c-clientmarkup">Dynamic relationships between age, amyloid-β deposition, and glucose metabolism link to the regional vulnerability to Alzheimer’s disease</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AOh%2C%20Hwamee">Oh, Hwamee</a>; </li><li><a href="/search/?q=author%3AMadison%2C%20Cindee">Madison, Cindee</a>; </li><li><a href="/search/?q=author%3ABaker%2C%20Suzanne">Baker, Suzanne</a>; </li><li><a href="/search/?q=author%3ARabinovici%2C%20Gil">Rabinovici, Gil</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AJagust%2C%20William">Jagust, William</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_postprints">UC Berkeley Previously Published Works</a> (2016)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">SEE HANSSON AND GOURAS DOI101093/AWW146 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Although some brain regions such as precuneus and lateral temporo-parietal cortex have been shown to be more vulnerable to Alzheimer's disease than other areas, a mechanism underlying the differential regional vulnerability to Alzheimer's disease remains to be elucidated. Using fluorodeoxyglucose and Pittsburgh compound B positron emission tomography imaging glucose metabolism and amyloid-β deposition, we tested whether and how life-long changes in glucose metabolism relate to amyloid-β deposition and Alzheimer's disease-related hypometabolism. Nine healthy young adults (age range: 20-30), 96 cognitively normal older adults (age range: 61-96), and 20 patients with Alzheimer's disease (age range: 50-90) were scanned using fluorodeoxyglucose and Pittsburgh compound B positron emission tomography. Among cognitively normal older subjects, 32 were further classified as amyloid-positive, with 64 as amyloid-negative. To assess the contribution of glucose metabolism to the regional vulnerability to amyloid-β deposition, we defined the highest and lowest metabolic regions in young adults and examined differences in amyloid deposition between these regions across groups. Two-way analyses of variance were conducted to assess regional differences in age and amyloid-β-related changes in glucose metabolism. Multiple regressions were applied to examine the association between amyloid-β deposition and regional glucose metabolism. Both region of interest and whole-brain voxelwise analyses were conducted to complement and confirm the results derived from the other approach. Regional differences in glucose metabolism between the highest and lowest metabolism regions defined in young adults (T = 12.85, P < 0.001) were maintained both in Pittsburgh compound B-negative cognitively normal older subjects (T = 6.66, P < 0.001) and Pittsburgh compound B-positive cognitively normal older subjects (T = 10.62, P < 0.001), but, only the Pittsburgh compound B-positive cognitively normal older subjects group showed significantly higher Pittsburgh compound B retention in the highest compared to the lowest glucose metabolism regions defined in young adults (T = 2.05, P < 0.05). Regional differences in age and amyloid-β-dependent changes in glucose metabolism were found such that frontal glucose metabolism was reduced with age, while glucose metabolism in the precuneus was maintained across the lifespan (right hemisphere: F = 7.69, P < 0.001; left hemisphere: F = 8.69, P < 0.001). Greater Alzheimer's disease-related hypometabolism was observed in brain regions that showed both age-invariance and amyloid-β-related increases in glucose metabolism. Our results indicate that although early and life-long regional variation in glucose metabolism relates to the regional vulnerability to amyloid-β accumulation, Alzheimer's disease-related hypometabolism is more specific to brain regions showing age-invariant glucose metabolism and amyloid-β-related hypermetabolism.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/9tr7d9gf"><div class="c-clientmarkup">Amyloid imaging, risk disclosure and Alzheimers disease: ethical and practical issues</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ARoberts%2C%20J%20Scott">Roberts, J Scott</a>; </li><li><a href="/search/?q=author%3ADunn%2C%20Laura%20B">Dunn, Laura B</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2013)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">PET ligands that bind with high specificity to amyloid plaques represent a major breakthrough in Alzheimer's disease (AD) research. Amyloid neuroimaging is now approved by the US FDA to aid in the diagnosis of AD, and is being used to identify amyloid-positive but asymptomatic individuals for secondary AD prevention trials. The use of amyloid neuroimaging in preclinical populations raises important ethical and practical challenges, including determining appropriate uses of this technology, evaluating the potential benefits and harms of disclosing results, and communicating effectively about testing with patients and family members. Emerging policy issues also require consideration (e.g., legal safeguards for biomarker-positive individuals). Further research is needed to inform effective and ethical implementation and regulation of amyloid imaging.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/9tr7d9gf"><img src="/cms-assets/4d9295de782dfdcfdd219f5a520284dfe5afddac02f5f2cba35b8837e3ef5e08" alt="Cover page: Amyloid imaging, risk disclosure and Alzheimers disease: ethical and practical issues"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/78z7x7vp"><div class="c-clientmarkup">Alzheimer's Disease Neurodegenerative Biomarkers Are Associated with Decreased Cognitive Function but Not β-Amyloid in Cognitively Normal Older Individuals</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AWirth%2C%20Miranka">Wirth, Miranka</a>; </li><li><a href="/search/?q=author%3AMadison%2C%20Cindee%20M">Madison, Cindee M</a>; </li><li><a href="/search/?q=author%3ARabinovici%2C%20Gil%20D">Rabinovici, Gil D</a>; </li><li><a href="/search/?q=author%3AOh%2C%20Hwamee">Oh, Hwamee</a>; </li><li><a href="/search/?q=author%3ALandau%2C%20Susan%20M">Landau, Susan M</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AJagust%2C%20William%20J">Jagust, William J</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2013)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">β-Amyloid (Aβ) plaque deposition and neurodegeneration within temporoparietal and hippocampal regions may indicate increased risk of Alzheimer's disease (AD). This study examined relationships between AD biomarkers of Aβ and neurodegeneration as well as cognitive performance in cognitively normal older individuals. Aβ burden was quantified in 72 normal older human subjects from the Berkeley Aging Cohort (BAC) using [(11)C] Pittsburgh compound B (PIB) positron emission tomography. In the same individuals, we measured hippocampal volume, as well as glucose metabolism and cortical thickness, which were extracted from a template of cortical AD-affected regions. The three functional and structural biomarkers were merged into a highly AD-sensitive multimodality biomarker reflecting neural integrity. In the normal older individuals, there was no association between elevated PIB uptake and either the single-modality or the multimodality neurodegenerative biomarkers. Lower neural integrity within the AD-affected regions and a control area (the visual cortex) was related to lower scores on memory and executive function tests; the same association was not found with PIB retention. The relationship between cognition and the multimodality AD biomarker was stronger in individuals with the highest PIB uptake. The findings indicate that neurodegeneration occurs within AD regions regardless of Aβ deposition and accounts for worse cognition in cognitively normal older people. The impact of neural integrity on cognitive functions is, however, enhanced in the presence of high Aβ burden for brain regions that are most affected in AD.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/78z7x7vp"><img src="/cms-assets/a0502b6c04576721e3ab3cc26aeb6ee2e72bccafdab9421be672e9d707a78db8" alt="Cover page: Alzheimer's Disease Neurodegenerative Biomarkers Are Associated with Decreased Cognitive Function but Not β-Amyloid in Cognitively Normal Older Individuals"/></a></div></section><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" 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Resources","type":"link"}]},{"id":10,"name":"UC Open Access Policies","slug":"ucoapolicies","type":"page","url":"/ucoapolicies"},{"id":12,"name":"eScholarship Publishing","slug":"publishing","type":"page","url":"/publishing"}],"social":{"facebook":null,"twitter":null,"rss":"/rss/unit/root"},"breadcrumb":[{"name":"eScholarship","id":"root","url":"/"}]},"campuses":[{"id":"","name":"eScholarship at..."},{"id":"ucb","name":"UC Berkeley"},{"id":"ucd","name":"UC Davis"},{"id":"uci","name":"UC Irvine"},{"id":"ucla","name":"UCLA"},{"id":"ucm","name":"UC Merced"},{"id":"ucr","name":"UC Riverside"},{"id":"ucsd","name":"UC San Diego"},{"id":"ucsf","name":"UCSF"},{"id":"ucsb","name":"UC Santa Barbara"},{"id":"ucsc","name":"UC Santa Cruz"},{"id":"ucop","name":"UC Office of the President"},{"id":"lbnl","name":"Lawrence Berkeley National Laboratory"},{"id":"anrcs","name":"UC Agriculture & Natural Resources"}],"query":{"q":"author:Rabinovici, Gil","sort":"rel","rows":"10","info_start":"0","start":"0","filters":{}},"count":239,"info_count":0,"infoResults":[],"searchResults":[{"id":"qt12v4b2m7","title":"Amyloid biomarkers: pushing the limits of early detection","abstract":"This scientific commentary refers to \u2018Cerebrospinal fluid analysis detects cerebral amyloid-\u03B2 accumulation earlier than positron emission tomography\u2019, by Palmqvist et al. (doi: 10.1093/brain/aww015 ).","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":158,"asset_id":"d1fda7de14fdd37565efdf6e1e8f65d508a283ddd36ba45579870affceba1541","timestamp":1683074837,"image_type":"png"},"pub_year":2016,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt7dp8c6v1","title":"Late-onset Alzheimer Disease.","abstract":"<h4>Purpose of review</h4>Alzheimer disease (AD) is the most common cause of late-onset dementia. This article describes the epidemiology, genetic and environmental risk factors, clinical diagnosis, biomarkers, and treatment of late-onset AD, defined by age of onset of 65 years or older.<h4>Recent findings</h4>An estimated 5.7 million Americans are living with AD dementia, with the number of affected individuals growing rapidly because of an aging population. Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease. The primary genetic risk factor for late-onset AD is the apolipoprotein E (APOE) \u03B54 allele. AD typically presents with early and prominent episodic memory loss, although this clinical syndrome is neither sensitive nor specific for underlying AD neuropathology. Emerging CSF and imaging biomarkers can now detect the key neuropathologic features of the disease (amyloid plaques, neurofibrillary tangles, and neurodegeneration) in living people, allowing for characterization of patients based on biological measures. A comprehensive treatment plan for AD includes use of symptomatic medications, optimal treatment of comorbid conditions and neuropsychiatric symptoms, counseling about safety and future planning, and referrals to community resources.<h4>Summary</h4>AD is very common in older neurologic patients. Neurologists should set the standard for the diagnosis and care of patients with AD and should be familiar with emerging biomarkers that have transformed AD research and are primed to enter the clinical arena.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":157,"asset_id":"2b14d424d7e1dfec284712aa2cbbf1f39d687f471a1216d0a289a8ba563f4929","timestamp":1685073645,"image_type":"png"},"pub_year":2019,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt4r41g6f8","title":"Amyloid imaging in the differential diagnosis of dementia: review and potential clinical applications","abstract":"In the past decade, positron emission tomography (PET) with carbon-11-labeled Pittsburgh Compound B (PIB) has revolutionized the neuroimaging of aging and dementia by enabling in vivo detection of amyloid plaques, a core pathologic feature of Alzheimer's disease (AD). Studies suggest that PIB-PET is sensitive for AD pathology, can distinguish AD from non-AD dementia (for example, frontotemporal lobar degeneration), and can help determine whether mild cognitive impairment is due to AD. Although the short half-life of the carbon-11 radiolabel has thus far limited the use of PIB to research, a second generation of tracers labeled with fluorine-18 has made it possible for amyloid PET to enter the clinical era. In the present review, we summarize the literature on amyloid imaging in a range of neurodegenerative conditions. We focus on potential clinical applications of amyloid PET and its role in the differential diagnosis of dementia. We suggest that amyloid imaging will be particularly useful in the evaluation of mildly affected, clinically atypical or early age-at-onset patients, and illustrate this with case vignettes from our practice. We emphasize that amyloid imaging should supplement (not replace) a detailed clinical evaluation. We caution against screening asymptomatic individuals, and discuss the limited positive predictive value in older populations. Finally, we review limitations and unresolved questions related to this exciting new technique.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Laforce, Robert","fname":"Robert","lname":"Laforce"},{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":175,"asset_id":"a4a8582d74842eb9192148646eef9cde37b0085ac04bad286c23ca16bd661dc7","timestamp":1589676016,"image_type":"png"},"pub_year":2011,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt6wq5r1p8","title":"Identifying degenerative effects of repetitive head trauma with neuroimaging: a clinically-oriented review","abstract":"<h4>Background and scope of review</h4>Varying severities and frequencies of head trauma may result in dynamic acute and chronic pathophysiologic responses in the brain. Heightened attention to long-term effects of head trauma, particularly repetitive head trauma, has sparked recent efforts to identify neuroimaging biomarkers of underlying disease processes. Imaging modalities like structural magnetic resonance imaging (MRI) and positron emission tomography (PET) are the most clinically applicable given their use in neurodegenerative disease diagnosis and differentiation. In recent years, researchers have targeted repetitive head trauma cohorts in hopes of identifying in vivo biomarkers for underlying biologic changes that might ultimately improve diagnosis of chronic traumatic encephalopathy (CTE) in living persons. These populations most often include collision sport athletes (e.g., American football, boxing) and military veterans with repetitive low-level blast exposure. We provide a clinically-oriented review of neuroimaging data from repetitive head trauma cohorts based on structural MRI, FDG-PET, A\u03B2-PET, and tau-PET. We supplement the review with two patient reports of neuropathology-confirmed, clinically impaired adults with prior repetitive head trauma who underwent structural MRI, FDG-PET, A\u03B2-PET, and tau-PET in addition to comprehensive clinical examinations before death.<h4>Review conclusions</h4>Group-level comparisons to controls without known head trauma have revealed inconsistent regional volume differences, with possible propensity for medial temporal, limbic, and subcortical (thalamus, corpus callosum) structures. Greater frequency and severity (i.e., length) of cavum septum pellucidum (CSP) is observed in repetitive head trauma cohorts compared to unexposed controls. It remains unclear whether CSP predicts a particular neurodegenerative process, but CSP presence should increase suspicion that clinical impairment is at least partly attributable to the individual's head trauma exposure (regardless of underlying disease). PET imaging similarly has not revealed a prototypical metabolic or molecular pattern associated with repetitive head trauma or predictive of CTE based on the most widely studied radiotracers. Given the range of clinical syndromes and neurodegenerative pathologies observed in a subset of adults with prior repetitive head trauma, structural MRI and PET imaging may still be useful for differential diagnosis (e.g., assessing suspected Alzheimer's disease).","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Asken, Breton M","email":"breton.asken@ucsf.edu","fname":"Breton M","lname":"Asken"},{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":175,"asset_id":"a425a32114cd6416bd5582c47b5fade3a5b06e877698f322f9c43b549179e045","timestamp":1623072409,"image_type":"png"},"pub_year":2021,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt2t12b939","title":"The Role of Amyloid PET in Imaging Neurodegenerative Disorders: A Review.","abstract":"Imaging of amyloid deposition using PET has been available in research studies for 2 decades and has been approved for clinical use by the U.S. Food and Drug Administration, the European Medicines Agency, and other regulatory agencies around the world. Amyloid PET is a crucial tool for the diagnosis of Alzheimer disease, as it allows the noninvasive detection of amyloid plaques, a core neuropathologic feature that defines the disease. The clinical use of amyloid PET is expected to increase with recent accelerated approval in the United States of aducanumab, an antiamyloid monoclonal antibody, for the treatment of mild cognitive impairment and mild dementia due to Alzheimer disease. However, amyloid pathology can also be found in cognitively unimpaired older adults and in patients with other neurodegenerative disorders. The aim of this review is to provide an up-to-date overview of the application of amyloid PET in neurodegenerative diseases. We provide an in-depth analysis of the clinical, pathologic, and imaging correlates; a comparison with other available biomarkers; and a review of the application of amyloid PET in clinical trials and clinical utility studies.","content_type":null,"author_hide":null,"authors":[{"name":"Chapleau, Marianne","email":"marianne.chapleau@ucsf.edu","fname":"Marianne","lname":"Chapleau"},{"name":"Iaccarino, Leonardo","fname":"Leonardo","lname":"Iaccarino","ORCID_id":"0000-0003-0053-9519"},{"name":"Soleimani-Meigooni, David","email":"david.soleimani-meigooni@ucsf.edu","fname":"David","lname":"Soleimani-Meigooni","ORCID_id":"0000-0003-4197-3039"},{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":null,"pub_year":2022,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt534865f3","title":"The Rise of Pseudomedicine for Dementia and Brain Health","abstract":null,"content_type":null,"author_hide":null,"authors":[{"name":"Hellmuth, Joanna","fname":"Joanna","lname":"Hellmuth"},{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"},{"name":"Miller, Bruce L","email":"bruce.miller@ucsf.edu","fname":"Bruce L","lname":"Miller","ORCID_id":"0000-0002-2152-4220"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":null,"pub_year":2019,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt00r0j5xb","title":"Executive Dysfunction","abstract":"<h4>Purpose of review</h4>Executive functions represent a constellation of cognitive abilities that drive goal-oriented behavior and are critical to the ability to adapt to an ever-changing world. This article provides a clinically oriented approach to classifying, localizing, diagnosing, and treating disorders of executive function, which are pervasive in clinical practice.<h4>Recent findings</h4>Executive functions can be split into four distinct components: working memory, inhibition, set shifting, and fluency. These components may be differentially affected in individual patients and act together to guide higher-order cognitive constructs such as planning and organization. Specific bedside and neuropsychological tests can be applied to evaluate components of executive function. While dysexecutive syndromes were first described in patients with frontal lesions, intact executive functioning relies on distributed neural networks that include not only the prefrontal cortex, but also the parietal cortex, basal ganglia, thalamus, and cerebellum. Executive dysfunction arises from injury to any of these regions, their white matter connections, or neurotransmitter systems. Dysexecutive symptoms therefore occur in most neurodegenerative diseases and in many other neurologic, psychiatric, and systemic illnesses. Management approaches are patient specific and should focus on treatment of the underlying cause in parallel with maximizing patient function and safety via occupational therapy and rehabilitation.<h4>Summary</h4>Executive dysfunction is extremely common in patients with neurologic disorders. Diagnosis and treatment hinge on familiarity with the clinical components and neuroanatomic correlates of these complex, high-order cognitive processes.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"},{"name":"Stephens, Melanie L","fname":"Melanie L","lname":"Stephens"},{"name":"Possin, Katherine L","fname":"Katherine L","lname":"Possin"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":156,"asset_id":"cfd51b0acfa8654a53e71c5672c257c094e9a74aa0748fb2301dee7309982fef","timestamp":1681758297,"image_type":"png"},"pub_year":2015,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt0099d4tn","title":"Dynamic relationships between age, amyloid-\u03B2 deposition, and glucose metabolism link to the regional vulnerability to Alzheimer\u2019s disease","abstract":"SEE HANSSON AND GOURAS DOI101093/AWW146 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Although some brain regions such as precuneus and lateral temporo-parietal cortex have been shown to be more vulnerable to Alzheimer's disease than other areas, a mechanism underlying the differential regional vulnerability to Alzheimer's disease remains to be elucidated. Using fluorodeoxyglucose and Pittsburgh compound B positron emission tomography imaging glucose metabolism and amyloid-\u03B2 deposition, we tested whether and how life-long changes in glucose metabolism relate to amyloid-\u03B2 deposition and Alzheimer's disease-related hypometabolism. Nine healthy young adults (age range: 20-30), 96 cognitively normal older adults (age range: 61-96), and 20 patients with Alzheimer's disease (age range: 50-90) were scanned using fluorodeoxyglucose and Pittsburgh compound B positron emission tomography. Among cognitively normal older subjects, 32 were further classified as amyloid-positive, with 64 as amyloid-negative. To assess the contribution of glucose metabolism to the regional vulnerability to amyloid-\u03B2 deposition, we defined the highest and lowest metabolic regions in young adults and examined differences in amyloid deposition between these regions across groups. Two-way analyses of variance were conducted to assess regional differences in age and amyloid-\u03B2-related changes in glucose metabolism. Multiple regressions were applied to examine the association between amyloid-\u03B2 deposition and regional glucose metabolism. Both region of interest and whole-brain voxelwise analyses were conducted to complement and confirm the results derived from the other approach. Regional differences in glucose metabolism between the highest and lowest metabolism regions defined in young adults (T = 12.85, P < 0.001) were maintained both in Pittsburgh compound B-negative cognitively normal older subjects (T = 6.66, P < 0.001) and Pittsburgh compound B-positive cognitively normal older subjects (T = 10.62, P < 0.001), but, only the Pittsburgh compound B-positive cognitively normal older subjects group showed significantly higher Pittsburgh compound B retention in the highest compared to the lowest glucose metabolism regions defined in young adults (T = 2.05, P < 0.05). Regional differences in age and amyloid-\u03B2-dependent changes in glucose metabolism were found such that frontal glucose metabolism was reduced with age, while glucose metabolism in the precuneus was maintained across the lifespan (right hemisphere: F = 7.69, P < 0.001; left hemisphere: F = 8.69, P < 0.001). Greater Alzheimer's disease-related hypometabolism was observed in brain regions that showed both age-invariance and amyloid-\u03B2-related increases in glucose metabolism. Our results indicate that although early and life-long regional variation in glucose metabolism relates to the regional vulnerability to amyloid-\u03B2 accumulation, Alzheimer's disease-related hypometabolism is more specific to brain regions showing age-invariant glucose metabolism and amyloid-\u03B2-related hypermetabolism.","content_type":null,"author_hide":null,"authors":[{"name":"Oh, Hwamee","fname":"Hwamee","lname":"Oh"},{"name":"Madison, Cindee","fname":"Cindee","lname":"Madison"},{"name":"Baker, Suzanne","email":"SLBaker@lbl.gov","fname":"Suzanne","lname":"Baker","ORCID_id":"0000-0003-0209-3127"},{"name":"Rabinovici, Gil","email":"gil.rabinovici@ucsf.edu","fname":"Gil","lname":"Rabinovici"},{"name":"Jagust, William","email":"jagust@berkeley.edu","fname":"William","lname":"Jagust"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":null,"pub_year":2016,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC Berkeley Previously Published Works","link_path":"ucb_postprints"}},{"id":"qt9tr7d9gf","title":"Amyloid imaging, risk disclosure and Alzheimers disease: ethical and practical issues","abstract":"PET ligands that bind with high specificity to amyloid plaques represent a major breakthrough in Alzheimer's disease (AD) research. Amyloid neuroimaging is now approved by the US FDA to aid in the diagnosis of AD, and is being used to identify amyloid-positive but asymptomatic individuals for secondary AD prevention trials. The use of amyloid neuroimaging in preclinical populations raises important ethical and practical challenges, including determining appropriate uses of this technology, evaluating the potential benefits and harms of disclosing results, and communicating effectively about testing with patients and family members. Emerging policy issues also require consideration (e.g., legal safeguards for biomarker-positive individuals). Further research is needed to inform effective and ethical implementation and regulation of amyloid imaging.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Roberts, J Scott","fname":"J Scott","lname":"Roberts"},{"name":"Dunn, Laura B","fname":"Laura B","lname":"Dunn"},{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":162,"asset_id":"4d9295de782dfdcfdd219f5a520284dfe5afddac02f5f2cba35b8837e3ef5e08","timestamp":1681796473,"image_type":"png"},"pub_year":2013,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt78z7x7vp","title":"Alzheimer's Disease Neurodegenerative Biomarkers Are Associated with Decreased Cognitive Function but Not \u03B2-Amyloid in Cognitively Normal Older Individuals","abstract":"\u03B2-Amyloid (A\u03B2) plaque deposition and neurodegeneration within temporoparietal and hippocampal regions may indicate increased risk of Alzheimer's disease (AD). This study examined relationships between AD biomarkers of A\u03B2 and neurodegeneration as well as cognitive performance in cognitively normal older individuals. A\u03B2 burden was quantified in 72 normal older human subjects from the Berkeley Aging Cohort (BAC) using [(11)C] Pittsburgh compound B (PIB) positron emission tomography. In the same individuals, we measured hippocampal volume, as well as glucose metabolism and cortical thickness, which were extracted from a template of cortical AD-affected regions. The three functional and structural biomarkers were merged into a highly AD-sensitive multimodality biomarker reflecting neural integrity. In the normal older individuals, there was no association between elevated PIB uptake and either the single-modality or the multimodality neurodegenerative biomarkers. Lower neural integrity within the AD-affected regions and a control area (the visual cortex) was related to lower scores on memory and executive function tests; the same association was not found with PIB retention. The relationship between cognition and the multimodality AD biomarker was stronger in individuals with the highest PIB uptake. The findings indicate that neurodegeneration occurs within AD regions regardless of A\u03B2 deposition and accounts for worse cognition in cognitively normal older people. The impact of neural integrity on cognitive functions is, however, enhanced in the presence of high A\u03B2 burden for brain regions that are most affected in AD.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Wirth, Miranka","fname":"Miranka","lname":"Wirth"},{"name":"Madison, Cindee M","fname":"Cindee M","lname":"Madison"},{"name":"Rabinovici, Gil D","email":"gil.rabinovici@ucsf.edu","fname":"Gil D","lname":"Rabinovici"},{"name":"Oh, Hwamee","fname":"Hwamee","lname":"Oh"},{"name":"Landau, Susan M","fname":"Susan M","lname":"Landau"},{"name":"Jagust, William J","email":"jagust@berkeley.edu","fname":"William J","lname":"Jagust"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":172,"asset_id":"a0502b6c04576721e3ab3cc26aeb6ee2e72bccafdab9421be672e9d707a78db8","timestamp":1680732830,"image_type":"png"},"pub_year":2013,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}}],"facets":[{"display":"Type of Work","fieldName":"type_of_work","facets":[{"value":"article","count":239,"displayName":"Article"},{"value":"monograph","count":0,"displayName":"Book"},{"value":"dissertation","count":0,"displayName":"Theses"},{"value":"multimedia","count":0,"displayName":"Multimedia"}]},{"display":"Peer Review","fieldName":"peer_reviewed","facets":[{"value":"1","count":239,"displayName":"Peer-reviewed only"}]},{"display":"Supplemental Material","fieldName":"supp_file_types","facets":[{"value":"video","count":0,"displayName":"Video"},{"value":"audio","count":0,"displayName":"Audio"},{"value":"images","count":0,"displayName":"Images"},{"value":"zip","count":0,"displayName":"Zip"},{"value":"other files","count":1,"displayName":"Other files"}]},{"display":"Publication Year","fieldName":"pub_year","range":{"pub_year_start":null,"pub_year_end":null}},{"display":"Campus","fieldName":"campuses","facets":[{"value":"ucb","count":45,"displayName":"UC Berkeley"},{"value":"ucd","count":8,"displayName":"UC Davis"},{"value":"uci","count":82,"displayName":"UC Irvine"},{"value":"ucla","count":153,"displayName":"UCLA"},{"value":"ucm","count":0,"displayName":"UC Merced"},{"value":"ucr","count":0,"displayName":"UC Riverside"},{"value":"ucsd","count":27,"displayName":"UC San Diego"},{"value":"ucsf","count":239,"displayName":"UCSF"},{"value":"ucsb","count":1,"displayName":"UC Santa Barbara"},{"value":"ucsc","count":9,"displayName":"UC Santa Cruz"},{"value":"ucop","count":32,"displayName":"UC Office of the President"},{"value":"lbnl","count":129,"displayName":"Lawrence Berkeley National Laboratory"},{"value":"anrcs","count":0,"displayName":"UC Agriculture & Natural Resources"}]},{"display":"Department","fieldName":"departments","facets":[{"value":"lbnl_bs","count":37,"displayName":"BioSciences"},{"value":"deb","count":13,"displayName":"Department of Epidemiology and Biostatistics"},{"value":"ucdavisneurology","count":7,"displayName":"Department of Neurology, UC Davis School of Medicine"},{"value":"rgpo","count":32,"displayName":"Research Grants Program Office"},{"value":"ucsdsom","count":25,"displayName":"School of Medicine"},{"value":"uclapsych","count":2,"displayName":"UCLA Department of Psychology"},{"value":"ucsflibrary","count":1,"displayName":"UCSF Library"}]},{"display":"Journal","fieldName":"journals","facets":[]},{"display":"Discipline","fieldName":"disciplines","facets":[{"value":"Medicine and Health Sciences","count":3}]},{"display":"Reuse License","fieldName":"rights","facets":[{"value":"CC BY","count":6,"displayName":"BY - Attribution required"},{"value":"CC BY-NC-ND","count":1,"displayName":"BY-NC-ND - Attribution; NonCommercial use; No derivatives"}]}]};</script> <script src="/js/vendors~app-bundle-7424603c338d723fd773.js"></script> <script src="/js/app-bundle-8362e6d7829414ab4baa.js"></script> </body> </html>