Author
Giovanni B. Frisoni
Other affiliations: Geneva College, University of Rome Tor Vergata, University of Bari ...read more
Bio: Giovanni B. Frisoni is an academic researcher from University of Geneva. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 101, co-authored 871 publications receiving 46199 citations. Previous affiliations of Giovanni B. Frisoni include Geneva College & University of Rome Tor Vergata.
Papers published on a yearly basis
Papers
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Pierre-and-Marie-Curie University1, French Institute of Health and Medical Research2, University of British Columbia3, UBC Hospital4, Beta5, Sahlgrenska University Hospital6, University of Virginia7, McGill University8, Brigham and Women's Hospital9, Washington University in St. Louis10, Vita-Salute San Raffaele University11, University College London12, University of Antwerp13, University of Geneva14, University of California, San Diego15, University of Kentucky16, Karolinska University Hospital17, university of lille18, University of California, San Francisco19, University of Nice Sophia Antipolis20, Brown University21, University of Paris22, Universidade Federal de Minas Gerais23, Maastricht University Medical Centre24, University of Southern California25, NewYork–Presbyterian Hospital26, VU University Amsterdam27, Lou Ruvo Brain Institute28
TL;DR: It is proposed that downstream topographical biomarkers of the disease, such as volumetric MRI and fluorodeoxyglucose PET, might better serve in the measurement and monitoring of the course of disease.
Abstract: In the past 8 years, both the International Working Group (IWG) and the US National Institute on Aging-Alzheimer's Association have contributed criteria for the diagnosis of Alzheimer's disease (AD) that better define clinical phenotypes and integrate biomarkers into the diagnostic process, covering the full staging of the disease. This Position Paper considers the strengths and limitations of the IWG research diagnostic criteria and proposes advances to improve the diagnostic framework. On the basis of these refinements, the diagnosis of AD can be simplified, requiring the presence of an appropriate clinical AD phenotype (typical or atypical) and a pathophysiological biomarker consistent with the presence of Alzheimer's pathology. We propose that downstream topographical biomarkers of the disease, such as volumetric MRI and fluorodeoxyglucose PET, might better serve in the measurement and monitoring of the course of disease. This paper also elaborates on the specific diagnostic criteria for atypical forms of AD, for mixed AD, and for the preclinical states of AD.
2,581 citations
Pierre-and-Marie-Curie University1, Bristol-Myers Squibb2, University of British Columbia3, Yale University4, University of California, Los Angeles5, University of Virginia6, French Institute of Health and Medical Research7, University College London8, University of California, San Diego9, McGill University10, Goethe University Frankfurt11, University of Kentucky12, Tohoku University13, Newcastle University14, University of Lille Nord de France15, University of Nice Sophia Antipolis16, Brown University17, NewYork–Presbyterian Hospital18, VU University Amsterdam19, Maastricht University Medical Centre20
TL;DR: This paper aims to advance the scientific discussion by providing broader diagnostic coverage of the AD clinical spectrum and by proposing a common lexicon as a point of reference for the clinical and research communities.
Abstract: Alzheimer's disease (AD) is classically defined as a dual clinicopathological entity. The recent advances in use of reliable biomarkers of AD that provide in-vivo evidence of the disease has stimulated the development of new research criteria that reconceptualise the diagnosis around both a specific pattern of cognitive changes and structural/biological evidence of Alzheimer's pathology. This new diagnostic framework has stimulated debate about the definition of AD and related conditions. The potential for drugs to intercede in the pathogenic cascade of the disease adds some urgency to this debate. This paper by the International Working Group for New Research Criteria for the Diagnosis of AD aims to advance the scientific discussion by providing broader diagnostic coverage of the AD clinical spectrum and by proposing a common lexicon as a point of reference for the clinical and research communities. The cornerstone of this lexicon is to consider AD solely as a clinical and symptomatic entity that encompasses both predementia and dementia phases.
1,776 citations
TL;DR: The utility of structural imaging and other markers will be increased by standardization of acquisition and analysis methods, and by development of robust algorithms for automated assessment, as well as by research into other imaging and nonimaging markers.
Abstract: Structural imaging based on magnetic resonance is an integral part of the clinical assessment of patients with suspected Alzheimer dementia. Prospective data on the natural history of change in structural markers from preclinical to overt stages of Alzheimer disease are radically changing how the disease is conceptualized, and will influence its future diagnosis and treatment. Atrophy of medial temporal structures is now considered to be a valid diagnostic marker at the mild cognitive impairment stage. Structural imaging is also included in diagnostic criteria for the most prevalent non-Alzheimer dementias, reflecting its value in differential diagnosis. In addition, rates of whole-brain and hippocampal atrophy are sensitive markers of neurodegeneration, and are increasingly used as outcome measures in trials of potentially disease-modifying therapies. Large multicenter studies are currently investigating the value of other imaging and nonimaging markers as adjuncts to clinical assessment in diagnosis and monitoring of progression. The utility of structural imaging and other markers will be increased by standardization of acquisition and analysis methods, and by development of robust algorithms for automated assessment.
1,572 citations
TL;DR: The APOE ε4 allele modulates brain function decades before any clinical or neurophysiological expression of neurodegenerative processes and could be explained by differences in memory performance, brain morphology, or resting cerebral blood flow.
Abstract: The APOE epsilon4 allele is a risk factor for late-life pathological changes that is also associated with anatomical and functional brain changes in middle-aged and elderly healthy subjects. We investigated structural and functional effects of the APOE polymorphism in 18 young healthy APOE epsilon4-carriers and 18 matched noncarriers (age range: 20-35 years). Brain activity was studied both at rest and during an encoding memory paradigm using blood oxygen level-dependent fMRI. Resting fMRI revealed increased "default mode network" (involving retrosplenial, medial temporal, and medial-prefrontal cortical areas) coactivation in epsilon4-carriers relative to noncarriers. The encoding task produced greater hippocampal activation in epsilon4-carriers relative to noncarriers. Neither result could be explained by differences in memory performance, brain morphology, or resting cerebral blood flow. The APOE epsilon4 allele modulates brain function decades before any clinical or neurophysiological expression of neurodegenerative processes.
1,555 citations
Pierre-and-Marie-Curie University1, AXA2, University of British Columbia3, VU University Medical Center4, University of Southern California5, University of Toulouse6, ICM Partners7, French Institute of Health and Medical Research8, Imperial College London9, University of Lübeck10, Sahlgrenska University Hospital11, Federal Institute for Drugs and Medical Devices12, UCL Institute of Neurology13, University of Bordeaux14, University of Geneva15, McGill University16, University of Paris17, University of Washington18, Karolinska University Hospital19, University of Eastern Finland20, University of North Texas Health Science Center21, University of California, San Francisco22, University of Melbourne23, Brown University24, Brigham and Women's Hospital25, Harvard University26, Alzheimer's Association27, Lou Ruvo Brain Institute28, Mayo Clinic29
TL;DR: An updated review of the literature and evidence on the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage of Alzheimer's disease are provided.
Abstract: During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum. Thanks to evolving biomarker research and substantial discoveries, it is now possible to identify the disease even at the preclinical stage before the occurrence of the first clinical symptoms. This preclinical stage of AD has become a major research focus as the field postulates that early intervention may offer the best chance of therapeutic success. To date, very little evidence is established on this "silent" stage of the disease. A clarification is needed about the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage. This article is aimed at addressing all the different issues by providing for each of them an updated review of the literature and evidence, with practical recommendations.
1,235 citations
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28 Jul 2005
TL;DR: PfPMP1）与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
18,940 citations
Johns Hopkins University1, Johns Hopkins University School of Medicine2, Mayo Clinic3, McGill University4, Harvard University5, University of California, Irvine6, University of Pittsburgh7, Columbia University Medical Center8, Eli Lilly and Company9, Washington University in St. Louis10, UCL Institute of Neurology11, VU University Medical Center12, Alzheimer's Association13, Northwestern University14, National Institutes of Health15
TL;DR: The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available.
Abstract: The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia.
13,710 citations
9,362 citations
Journal Article•
9,185 citations
TL;DR: In this paper, a technique for automatically assigning a neuroanatomical label to each voxel in an MRI volume based on probabilistic information automatically estimated from a manually labeled training set is presented.
7,120 citations