Gil D. Rabinovici

ORCID: 0000-0002-3626-4265
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About
Contact & Profiles
Research Areas
  • Dementia and Cognitive Impairment Research
  • Alzheimer's disease research and treatments
  • Functional Brain Connectivity Studies
  • Advanced Neuroimaging Techniques and Applications
  • Medical Imaging Techniques and Applications
  • Parkinson's Disease Mechanisms and Treatments
  • Health Systems, Economic Evaluations, Quality of Life
  • Neurological Disease Mechanisms and Treatments
  • Health, Environment, Cognitive Aging
  • Amyotrophic Lateral Sclerosis Research
  • Neurobiology of Language and Bilingualism
  • Traumatic Brain Injury Research
  • S100 Proteins and Annexins
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Advanced MRI Techniques and Applications
  • Diet and metabolism studies
  • Cerebrovascular and Carotid Artery Diseases
  • Cholinesterase and Neurodegenerative Diseases
  • EEG and Brain-Computer Interfaces
  • Neural dynamics and brain function
  • Neurological Disorders and Treatments
  • Radiomics and Machine Learning in Medical Imaging
  • Cancer-related cognitive impairment studies
  • Epilepsy research and treatment
  • Memory and Neural Mechanisms

University of California, San Francisco
2016-2025

University of California System
2019-2025

University Memory and Aging Center
2016-2025

Alzheimer’s Disease Neuroimaging Initiative
2023-2025

Lawrence Berkeley National Laboratory
2015-2024

Center for Neurosciences
2017-2024

The University of Texas Health Science Center at Houston
2024

University of Florida
2024

University of Gothenburg
2020-2024

Boston University
2024

Background: PSP is a neuropathologically defined disease entity. Clinical diagnostic criteria, published in 1996 by the National Institute of Neurological Disorders and Stroke/Society for PSP, have excellent specificity, but their sensitivity limited variant syndromes with presentations other than Richardson's syndrome. Objective: We aimed to provide an evidence- consensus-based revision clinical criteria PSP. Methods: searched PubMed, Cochrane, Medline, PSYCInfo databases articles English...

10.1002/mds.26987 article EN Movement Disorders 2017-05-03

SEE SARAZIN ET AL DOI101093/BRAIN/AWW041 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: The advent of the positron emission tomography tracer (18)F-AV1451 provides unique opportunity to visualize regional distribution tau pathology in living human brain. In this study, we tested hypothesis that is closely linked symptomatology and patterns glucose hypometabolism Alzheimer's disease, contrast more diffuse amyloid-β pathology. We included 20 patients meeting criteria for probable disease...

10.1093/brain/aww027 article EN Brain 2016-03-08

Resting-state or intrinsic connectivity network functional magnetic resonance imaging provides a new tool for mapping large-scale neural function and dysfunction. Recently, we showed that behavioural variant frontotemporal dementia Alzheimer's disease cause atrophy within two major networks, an anterior 'Salience Network' (atrophied in dementia) posterior 'Default Mode disease). These networks exhibit anti-correlated relationship with each other the healthy brain. The diseases also feature...

10.1093/brain/awq075 article EN Brain 2010-04-21

Although beta-amyloid (Abeta) plaques are a primary diagnostic criterion for Alzheimer's disease, this pathology is commonly observed in the brains of non-demented older individuals. To explore importance absence dementia, we compared levels amyloid deposition (via 'Pittsburgh Compound-B' (PIB) positron emission tomography (PET) imaging) to hippocampus volume (HV) and episodic memory (EM) three groups: (i) normal controls (NC) from Berkeley Aging Cohort (BAC NC, n = 20); (ii) disease...

10.1093/brain/awn320 article EN Brain 2008-11-28

Epileptic activity associated with Alzheimer disease (AD) deserves increased attention because it has a harmful impact on these patients, can easily go unrecognized and untreated, may reflect pathogenic processes that also contribute to other aspects of the illness. We report key features AD-related seizures epileptiform are instructive for clinical practice highlight similarities between AD transgenic animal models disease.To describe common characteristics treatment outcomes patients...

10.1001/jamaneurol.2013.136 article EN JAMA Neurology 2013-07-08

Neuropathological and in vivo studies have revealed a tight relationship between tau pathology cognitive impairment across the Alzheimer's disease spectrum. However, is also intimately associated with neurodegeneration amyloid pathology. The aim of present study was therefore to assess whether grey matter atrophy contribute pathology, as measured 18F-AV-1451-PET imaging, deficits disease. We included 40 amyloid-positive patients meeting criteria for mild due (n = 5) or probable dementia 35)....

10.1093/brain/awx243 article EN Brain 2017-09-05

<h3>Importance</h3> Amyloid positron emission tomography (PET) detects amyloid plaques in the brain, a core neuropathological feature of Alzheimer disease. <h3>Objective</h3> To determine if PET is associated with subsequent changes management patients mild cognitive impairment (MCI) or dementia uncertain etiology. <h3>Design, Setting, and Participants</h3> The Imaging Dementia—Evidence for Scanning (IDEAS) study was single-group, multisite longitudinal that assessed association between...

10.1001/jama.2019.2000 article EN JAMA 2019-04-02

Abstract Objective Alzheimer's disease (AD) is found at autopsy in up to one third of patients with primary progressive aphasia (PPA), but clinical features that predict AD pathology PPA are not well defined. We studied the relationships between language presentation, Aβ amyloidosis, and glucose metabolism three variants using [ 11 C]‐Pittsburgh compound B ([ C]PIB) 18 F]‐labeled fluorodeoxyglucose positron emission tomography F]FDG‐PET). Methods Patients meeting criteria (N = 15) were...

10.1002/ana.21451 article EN Annals of Neurology 2008-10-01

A 'frontal variant of Alzheimer's disease' has been described in patients with predominant behavioural or dysexecutive deficits caused by disease pathology. The description this rare phenotype limited to case reports and small series, many clinical, neuroimaging neuropathological characteristics are not well understood. In retrospective study, we included 55 a behavioural-predominant presentation (behavioural disease) diagnosis high-likelihood (n = 17) and/or biomarker evidence pathology...

10.1093/brain/awv191 article EN Brain 2015-07-02

To characterize cognitive and behavioral features, physical findings, brain atrophy patterns in pathology-proven corticobasal degeneration (CBD) syndrome (CBS) with known histopathology.We reviewed clinical magnetic resonance imaging data all patients evaluated at our center either an autopsy diagnosis of CBD (n = 18) or CBS first presentation histopathology 40). Atrophy were compared using voxel-based morphometry.CBD was associated 4 syndromes: progressive nonfluent aphasia 5), variant...

10.1002/ana.22424 article EN Annals of Neurology 2011-03-16
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