Bruce L. Miller

ORCID: 0000-0002-2152-4220
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About
Contact & Profiles
Research Areas
  • Dementia and Cognitive Impairment Research
  • Alzheimer's disease research and treatments
  • Amyotrophic Lateral Sclerosis Research
  • Functional Brain Connectivity Studies
  • Parkinson's Disease Mechanisms and Treatments
  • Neurobiology of Language and Bilingualism
  • Advanced Neuroimaging Techniques and Applications
  • Neurological Disease Mechanisms and Treatments
  • Neurological diseases and metabolism
  • Memory and Neural Mechanisms
  • Prion Diseases and Protein Misfolding
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Spatial Neglect and Hemispheric Dysfunction
  • Advanced MRI Techniques and Applications
  • Genetic Neurodegenerative Diseases
  • EEG and Brain-Computer Interfaces
  • Epilepsy research and treatment
  • Neurological disorders and treatments
  • Health, Environment, Cognitive Aging
  • Action Observation and Synchronization
  • Neurogenetic and Muscular Disorders Research
  • S100 Proteins and Annexins
  • Cholinesterase and Neurodegenerative Diseases
  • Genetic Associations and Epidemiology
  • Neural dynamics and brain function

University Memory and Aging Center
2016-2025

University of California, San Francisco
2016-2025

Global Brain Health Institute
2017-2025

Trinity College Dublin
2019-2025

San Francisco VA Medical Center
2004-2024

Center for Neurosciences
2013-2024

The University of Texas Health Science Center at Houston
2024

University of Florida
2024

Alzheimer’s Disease Neuroimaging Initiative
2012-2024

Amsterdam University of Applied Sciences
2024

Ubiquitin-positive, tau- and α-synuclein–negative inclusions are hallmarks of frontotemporal lobar degeneration with ubiquitin-positive amyotrophic lateral sclerosis. Although the identity ubiquitinated protein specific to either disorder was unknown, we showed that TDP-43 is major disease in both disorders. Pathologic hyper-phosphorylated, ubiquitinated, cleaved generate C-terminal fragments recovered only from affected central nervous system regions, including hippocampus, neocortex,...

10.1126/science.1134108 article EN Science 2006-10-06

This article provides a classification of primary progressive aphasia (PPA) and its 3 main variants to improve the uniformity case reporting reliability research results. Criteria for PPA--nonfluent/agrammatic, semantic, logopenic--were developed by an international group PPA investigators who convened on occasions operationalize earlier published clinical descriptions subtypes. Patients are first diagnosed with then divided into based specific speech language features characteristic each...

10.1212/wnl.0b013e31821103e6 article EN Neurology 2011-02-17

Current criteria for the clinical diagnosis of pathologically confirmed corticobasal degeneration (CBD) no longer reflect expanding understanding this disease and its clinicopathologic correlations. An international consortium behavioral neurology, neuropsychology, movement disorders specialists developed new based on consensus a systematic literature review. Clinical diagnoses (early or late) were identified 267 nonoverlapping CBD cases from published reports brain banks. Combined with...

10.1212/wnl.0b013e31827f0fd1 article EN Neurology 2013-01-29

Abstract We performed a comprehensive cognitive, neuroimaging, and genetic study of 31 patients with primary progressive aphasia (PPA), decline in language functions that remains isolated for at least 2 years. Detailed speech evaluation was used to identify three different clinical variants: nonfluent (NFPA; n = 11), semantic dementia (SD; 10), third variant termed logopenic (LPA; 10). Voxel‐based morphometry (VBM) on MRIs showed that, when all PPA were analyzed together, the left...

10.1002/ana.10825 article EN Annals of Neurology 2004-02-03
William C. Nierman Arnab Pain Michael J. Anderson Jennifer R. Wortman Sun Kim and 93 more Javier Arroyo Matthew Berriman Keietsu Abe David B. Archer Clara Bermejo Joan W. Bennett Paul Bowyer Dan Chen Matthew Collins Richard Coulsen Robert M. Davies Paul S. Dyer Mark Farman Nadia Fedorova Natalie D. Fedorova Tamara V. Feldblyum Rainer Fischer Nigel Fosker Audrey Fraser José L. Garcı́a Maria J. García Arlette Goble Gustavo H. Goldman Katsuya Gomi Sam Griffiths‐Jones Ryan Gwilliam Brian J. Haas Hubertus Haas David Harris Hiroyuki Horiuchi Jiaqi Huang Sean Humphray Javier Jiménez Nancy P. Keller Hoda Khouri Katsuhiko Kitamoto Tetsuo Kobayashi Sven Konzack Resham Kulkarni Toshitaka Kumagai Anne Lafton Jean‐Paul Latgé Weixi Li Angela Lord Charles Lu William H. Majoros Gregory S. May Bruce L. Miller Yasmin A. Mohamoud Marı́a Molina Michel Monod Isabelle Mouyna Stephanie Mulligan Lee Murphy Susan O’Neil Ian T. Paulsen Miguel Á. Peñalva Mihaela Pertea Claire Price Bethan Pritchard Michael A. Quail Ester Rabbinowitsch Neil Rawlins Marie-Adele Rajandream Utz Reichard Hubert Renauld Geoffrey D. Robson Santiago Rodrı́guez de Córdoba José M. Rodríguez-Peña Catherine M. Ronning Simon Rutter Steven L. Salzberg Miguel Sánchez Juan C. Sánchez-Ferrero David Saunders Kathy Seeger Rob Squares Steven Squares Michio Takeuchi Fredj Tekaia Geoffrey Turner Carlos R. Vázquez de Aldana Janice F. Weidman Owen White John R. Woodward Jae‐Hyuk Yu Claire M. Fraser James E. Galagan Kiyoshi Asai Masayuki Machida Neil Hall Bart Barrell David W. Denning

10.1038/nature04332 article EN Nature 2005-12-21

<b><i>Objective: </i></b> To update the 1994 practice parameter for diagnosis of dementia in elderly. <b><i>Background:</i></b> The AAN previously published a on 1994. New research and clinical developments warrant an some aspects diagnosis. <b><i>Methods:</i></b> Studies English from 1985 through 1999 were identified that addressed four questions: 1) Are current criteria reliable? 2) diagnostic able to establish prevalent dementias elderly? 3) Do laboratory tests improve accuracy dementing...

10.1212/wnl.56.9.1143 article EN Neurology 2001-05-08

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

<b><i>Objective:</i></b> To identify and compare the patterns of cerebral atrophy associated with two clinical variants frontotemporal lobar degeneration (FTLD): dementia (FTD) semantic (SemD). <b><i>Methods:</i></b> Twenty patients FTLD were classified as having FTD (N = 8) or SemD 12) based on current criteria. Both groups showed a similar spectrum behavioral abnormalities, indicated by neuropsychiatric inventory. T1-weighted MRI was obtained for each patient 20 control subjects. The...

10.1212/wnl.58.2.198 article EN Neurology 2002-01-22

Background Proteins pathogenic in Alzheimer's disease (AD) were extracted from neurally derived blood exosomes and quantified to develop biomarkers for the staging of sporadic AD. Methods Blood obtained at one time-point patients with AD (n = 57) or frontotemporal dementia (FTD) 16), two time-points others 24) when cognitively normal 1 10 years later diagnosed enriched neural sources by immunoabsorption. AD-pathogenic exosomal proteins enzyme-linked immunosorbent assays. Results Mean levels...

10.1016/j.jalz.2014.06.008 article EN Alzheimer s & Dementia 2014-08-14

Abstract In this clinical study, the cerebrospinal fluid (CSF) level of a Novemberel form β‐amyloid peptide (Aβ) extending to position 42 (Aβ ) was determined in patients with Alzheimer's disease (AD) as well controls. addition measurement CSF Aβ levels, total peptides, microtubule‐associated protein τ, and apolipoprotein E (ApoE) genotype were also assessed. It is interesting that levels found be significantly lower AD relative controls, whereas not. has recently been shown preferentially...

10.1002/ana.410380413 article EN Annals of Neurology 1995-10-01

Patients with frontotemporal dementia (FTD) no known diagnosis of ALS or family history were clinically and electrophysiologically assessed for the presence ALS. Of 36 patients studied, five met criteria a definite two had EMG findings suggestive denervation in one limb. An additional prominent fasciculations six other trouble swallowing but all normal results on studies. One study progressed to over course 1 year.

10.1212/wnl.59.7.1077 article EN Neurology 2002-10-08
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