PHS 398 (Rev. 11/07), Biographical Sketch Format Page



| |

|BIOGRAPHICAL SKETCH |

|NAME |POSITION TITLE |

|Bradford C. Dickerson, M.D., M.MSc. |Associate Professor of Neurology, |

| |Harvard Medical School |

|eRA COMMONS USER NAME (credential, e.g., agency login) | |

|BCDICKERSON | |

|EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.) |

|INSTITUTION AND LOCATION |DEGREE |YEAR(s) |FIELD OF STUDY |

|Southern Methodist University, Dallas, TX |B.S. |1990 |Biomedical Engineering |

|Univ. of Illinois at Chicago College Of Medicine |M.D. |1994-1999 |Medicine |

|Brigham & Women’s Hospital, Boston, MA | |1999-2000 |Internship, Medicine |

|Massachusetts General & Brigham & Women's Hospitals | |2000-2003 |Residency, Neurology |

|Harvard-Martinos Center for Biomedical Imaging, MGH | |2003-2005 |Fellowship, Neuroimaging |

|Harvard-Brigham Behavioral Neurology Unit | |2003-2005 |Fellowship, Cognitive and Behavioral |

| | | |Neurology |

|Harvard Medical School/MIT, Boston, MA |M.Sc. |2003-2005 |Clinical Investigation |

A. Personal Statement

With more than 15 years of experience, I have a broad background in cognitive and behavioral neurology (including not only neurodegenerative diseases such as Alzheimer’s disease but also normal aging), neuroimaging, and cognitive-affective neuroscience (including memory, executive function and attention, language, emotion, and social cognition). As PI or Co-Investigator on multiple prior foundation-, industry- and NIH-funded grants, I have developed an approach using novel imaging and behavioral measures to study memory, executive, language, and affective brain systems across the lifespan from young adulthood to old age and in patients with neurologic or psychiatric disorders. In addition, I successfully administered these projects, collaborated with other researchers, and produced a number of peer-reviewed publications from each project. As Director of the MGH FTD Unit, Director of the MGH Center for Translational Brain Mapping, and Co-Director of the Imaging Core of the Alzheimer’s Disease Research Center, I am well-positioned to make use of imaging resources at MGH.

B. Positions and Honors

1990-1994 Manager, Information Program, Med/Sci Division, Alzheimer’s Assn, Chicago, IL

1995 Walter Rice Craig Research Fellow, Beckman Institute Neural Systems Group, Univ. of Illinois at Urbana-Champaign, Urbana, IL (Bill Greenough, mentor)

1996-97 Research Fellow, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL (Frank Morrell & Leyla deToledo-Morrell, mentors)

2002-2003 Chief Resident, Departments of Neurology, MGH and BWH, Boston, MA

2003- Assistant in Neurology, Massachusetts General Hospital, Boston, MA

2003-2006 Instructor in Neurology, Harvard Medical School, Boston, MA

2005- Co-Director, Neuroimaging Group, MGH Gerontology Research Unit, Charlestown, MA

2005- Director of Clinical Applications, MGH Morphometry Analysis Center, Charlestown, MA

2006-2008 Assistant Professor of Neurology, Harvard Medical School, Boston, MA

2007- Co-Director, Imaging Subcore, MGH Alzheimer’s Disease Research Center

2008- Director, MGH Frontotemporal Dementia Unit

2008- Associate Professor of Neurology, Harvard Medical School

2009- Co-Director, MGH Center for Neural Systems Investigations (CNSi)

2013- Rickles Endowed Chair in PPA/FTD Research, Massachusetts General Hospital, Boston, MA

2015- Director, MGH Center for Translational Brain Mapping, Boston, MA

Other Experience and Professional Memberships

1995- Society for Neuroscience

2001- American Academy of Neurology; Organization for Human Brain Mapping

2004- Greater Boston Alzheimer’s Association Medical & Scientific Advisory Board

2004- Member, grant review committees, multiple private foundations, including Fidelity Research Foundation, Alzheimer’s Association, Association for FTD

2004- Member, Society for Behavioral and Cognitive Neurology

2005- Member, grant review committees, multiple federal agencies, including National Science Foundation, NAME NIH Study Section, NIH Challenge Grant Review Panel #10 ZRG1 BDA-A

2005- Founding Chair, Charles River Association for Memory (with Dan Schacter, Howard Eichenbaum, John Gabrieli; we have held biannual meetings of 80-100 attendees )

2007- Editorial Board member, Hippocampus, Frontiers in Neuroscience, Neurodegenerative Disease Management, The Open Neurology Journal, Neuroimage: Clinical

2008- Member, grant review committees, multiple international federal agencies, including Canadian Institute for Health Research, Italian Ministry of Health, Ireland Health Research Board, Netherlands Organization for Scientific Research, UK Medical Research Council

2009- Faculty Member, Harvard FAS Mind/Brain/Behavior committee

2009- Director, Primer of Behavioral Neurology Annual CME Course, American Academy of Neurology

2010- Co-Director, Ånnual Harvard Dementia CME Course

2010- Member, Association for Frontotemporal Dementia Medical Advisory Board

2012- Chair, External Advisory Committee, Conte Center Grant P50 MH 094263, Prefrontal and Medial-Temporal Interactions in Memory, PI Howard Eichenbaum

2015- Associate Editor, Behavioral Neurology Section, Cortex

Honors

1995 Walter Rice Craig Summer Research Fellowship, Univ. of Illinois at Urbana-Champaign

1995-99 James Scholar, UIC College of Medicine

1996 Honorable Mention, UIC College of Medicine Student Research Symposium

1997 Second place, Sigma Xi Session of Rush University Research Forum

1998 Alpha Omega Alpha

1999 David M. Olkon Honors Scholarship, UIC College of Medicine

2001 Outstanding Resident Teacher in Neurology, Harvard Medical School

2002 Partners in Excellence Award (Neurology Chief Residents), Partners Healthcare System

2005 Mentor of the Year Award, Partners Neurology Residents

2013 Norman Geschwind Award in Behavioral Neurology, American Academy of Neurology

2014 Honorable Mention, Schwartz Center Compassionate Care Award

C. Contribution to Science

1. The convergence of computational imaging neuroscience and clinical neurology: Neurodegenerative disease signatures of regional atrophy


Drawing on my background in bioengineering and neuroanatomy, I have collaborated with imaging and computer scientists at the Martinos Center for Biomedical Imaging and anatomists at MGH and BU over the past 10 years to develop a novel computational approach to the detection of “disease signature” effects on neuroanatomy and brain function. We identified a “cortical signature of AD”—a distributed set of cerebral cortical regions in large-scale cognitive networks that undergo neurodegenerative atrophy in early AD, and showed that it is highly reliable in independent samples and is a clinically valid indicator of symptom severity (Dickerson et al., 2009). It is detectable in individuals with mild cognitive impairment symptoms prior to dementia, and predicts progression to AD dementia. We then showed in a series of studies that this marker could detect AD-related neuroanatomical changes in cognitively normal (CN) older adults with imaging evidence of brain amyloid (Dickerson et al., 2009). Before this report, it had not been thought that structural MRI could detect neuroanatomical abnormalities at such an early preclinical stage of AD. Yet, as is still true for many samples of elderly adults with “positive” amyloid PET scans, we do not know long-term outcome; some may live for years without symptoms and ultimately die with “silent” AD pathology.

Therefore, we took advantage of our relatively rare sample of CN adults who have been followed for more than a decade after MRI scanning, and collaborated with Rush University investigators who have a similar sample. We found support for the hypothesis that the AD-signature biomarker is detectable in CN older adults who eventually develop AD dementia nearly 10 years after scanning (Dickerson et al., 2011). A follow-up study in a new sample of CN older adults showed that the AD-signature MRI biomarker was not only useful for predicting cognitive decline but also a non-invasive, cost-effective indicator that positive individuals would be more likely to harbor AD-like amyloid levels in cerebrospinal fluid (Dickerson et al., 2012).

In a related line of high impact work, we have investigated these neuroimaging measures in the context of the genetic factors related to AD. We determined that very mild/prodromal AD carriers of the higher risk allele, APOE-ε4, expressed a more prominent memory deficit and cortical atrophy in large-scale memory circuits within the AD-signature than non-carriers of this risk allele. In contrast, non-carriers expressed a more prominent deficit in attention/executive function and cortical atrophy in attention/executive circuits within the AD-signature than carriers (Wolk et al., 2010). This finding—since replicated by other groups—indicates that APOE genotype modifies the selective vulnerability of specific large-scale neural networks to AD pathology.

Dickerson BC, Bakkour A, Salat DH, Greve DN, Grodstein F, Blacker D, Sperling RA, Atri A, Growdon JH, Hyman BT, Morris JC, Fischl B, Buckner RL (2009) The cortical signature of Alzheimer's disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. Cereb Cortex 19:497-510. PMCID: PMC2638813

Dickerson BC, Stoub TR, Shah RC, Sperling RA, Killiany RJ, Albert MS, Hyman BT, Blacker D, Detoledo- Morrell L (2011) Alzheimer-signature MRI biomarker predicts AD dementia in cognitively normal adults. Neurology 76:1395-1402. PMCID: PMC3087406

Dickerson BC, Wolk DA, On behalf of ADNI (2012) MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults. Neurology 78:84-90. PMCID:PMC3466670

Wolk DA, Dickerson BC, Alzheimer's Disease Neuroimaging I (2010) Apolipoprotein E (APOE) genotype has dissociable effects on memory and attentional-executive network function in Alzheimer's disease. Proc Natl Acad Sci U S A 107:10256-10261. PMCID: PMC2890481

2. Large-scale neural network connectivity and behavior

In the past 10 years, novel imaging and analytic technology has been developed to measure connectivity within large-scale neural networks using fMRI. We have used it to study the neural basis of individual differences in a variety of behaviors in healthy adults, including memory, emotion, and social behavior. We have also shown that the strength of connectivity within the large-scale memory circuit relates to memory abilities in healthy older adults (Wang et al., 2010), and that connectivity is disrupted in patients with early AD.

In a series of experiments conducted with Dr. Lisa Feldman Barrett, we investigated the neuroanatomic and neural network basis of individual differences in affective and social abilities, and how these abilities are lost in individuals in whom these circuits are disrupted as a result of Frontotemporal Dementia (FTD). First, we reported that normal individuals with larger amygdala size—relative to their brain size as a whole—had larger and more complex social networks than those with smaller amygdala (Bickart et al., 2011). We then used the new functional connectivity methods in a new study to demonstrate, for the first time, 1) the existence of three major large-scale neural networks converging on the amygdala which contribute importantly to social behavior; and 2) that 2 of these 3 networks influence the size of an individual’s social network (Bickart et al., 2012). In this paper, we made specific predictions about the functions of these networks and how social behavior would be disrupted by lesions to these networks. We then tested these hypotheses in a group of patients with FTD, showing that patients with more prominent neurodegenerative abnormalities in each of these networks have more prominent symptoms within the predicted social domains (Bickart et al., 2014). As part of this study, we developed a novel clinical instrument—the Social Impairment Rating Scale (SIRS)—which enables clinicians to grade the types and severity of social impairment in patients with this disease.

Bickart KC, Hollenbeck MC, Barrett LF, Dickerson BC (2012) Intrinsic amygdala-cortical functional connectivity predicts social network size in humans. J Neurosci 32:14729-14741. PMCID: PMC3569519

Bickart KC, Wright CI, Dautoff RJ, Dickerson BC, Barrett LF (2011) Amygdala volume and social network size in humans. Nat Neurosci 14:163-164. PMCID: PMC3079404

Bickart KC, Brickhouse M, Negreira A, Sapolsky D, Barrett LF, Dickerson BC (2014) Atrophy in distinct corticolimbic networks in frontotemporal dementia relates to social impairments measured using the Social Impairment Rating Scale. J Neurol Neurosurg Psychiatry 85:438-448. PMCID in process

Wang L, Laviolette P, O'Keefe K, Putcha D, Bakkour A, Van Dijk KR, Pihlajamaki M, Dickerson BC, Sperling RA (2010) Intrinsic connectivity between the hippocampus and posteromedial cortex predicts memory performance in cognitively intact older individuals. Neuroimage 51:910-917. PMCID: PMC2856812

3. Functional MRI studies of memory circuit function in aging and Alzheimer’s disease

In addition to these neuroanatomical and molecular measures, my colleagues and I performed a series of functional MRI (fMRI) studies of memory circuit function in aging and early AD. We showed that the degree to which portions of the large-scale memory circuit activates during learning determines whether cognitively intact older individuals will perform relatively well or relatively poorly on a memory task (Miller et al., 2008b). In a highly cited series of studies, we were the first to show that individuals with MCI hyperactivate portions of their memory circuit while learning new information, and that this hyperactivation is associated with more rapid clinical decline (Dickerson et al., 2004; Dickerson et al., 2005; Miller et al., 2008a). We later brought this work together with the AD signature studies described above to show that memory circuit hyperactivation correlates with the severity of AD-related cortical atrophy (Putcha et al., 2011), suggesting that it is a specific marker of inefficient synaptic function occurring in the setting of AD neuropathology.

Dickerson BC, Salat DH, Greve DN, Chua EF, Rand-Giovannetti E, Rentz DM, Bertram L, Mullin K, Tanzi RE, Blacker D, Albert MS, Sperling RA (2005) Increased hippocampal activation in mild cognitive impairment compared to normal aging and AD. Neurology 65:404-411. PMCID in process

Miller SL, Blacker D, Sperling RA, Dickerson BC (2008a) Hippocampal activation in adults with MCI predicts subsequent cognitive decline. J Neurol Neurosurg Psychiatry 79:630-635. PMCID: PMC2683145

Miller SL, Celone K, DePeau K, Diamond E, Dickerson BC, Rentz D, Pihlajamaki M, Sperling RA (2008b) Age-related memory impairment associated with loss of parietal deactivation but preserved hippocampal activation. Proc Natl Acad Sci U S A 105:2181-2186. PMCID: PMC2538895

Putcha D, Brickhouse M, O'Keefe K, Sullivan C, Rentz D, Marshall G, Dickerson B, Sperling R (2011) Hippocampal hyperactivation associated with cortical thinning in Alzheimer's disease signature regions in non-demented elderly adults. J Neurosci 31:17680-17688. PMCID:PMC3289551

4. Anatomical, psycholinguistic, and clinical studies of Primary Progressive Aphasia

I founded the MGH Harvard Primary Progressive Aphasia Clinical Research Program in 2007, and have since developed this program into an internationally recognized leader in PPA care and research. One of our major contributions to the field was the development (working closely with Drs. Marsel Mesulam and Sandra Weintraub) of a new scale for the assessment of language impairment in PPA (the Progressive Aphasia Severity Scale, aka PASS) as well as new MRI markers for diagnosis and monitoring of PPA, including a “PPA Signature” of cortical atrophy (Sapolsky et al., 2010; Sapolsky et al., 2014), inspired by our work on the AD Signature. The PPA Program’s Speech Pathologist, Daisy Hochberg, led this effort and has been working to train speech pathologists in the local area and around the country and in other countries (France, England, Australia) to use this new scale in working with patients to better measure their strengths and weaknesses, with the hope that this will help measure the effects of various types of attempted treatments. In our clinical research efforts, we recently described a novel clinical subtype of PPA (Perez et al., 2013). I am a founding member of the International PPA Connection (), the international clinical research registry for patients and investigators. In part as a result of these clinical research efforts, I was honored by being invited to edit Cambridge University Press’s forthcoming second edition of the leading textbook on PPA and FTD, which I named Hodges’ Frontotemporal Dementia (Dickerson, 2015) in tribute to Professor John Hodges who edited the first edition of the book. I also co-edited a 2014 Oxford University Press book, Dementia: Comprehensive Principles and Practice (Dickerson and Atri, 2014).

Sapolsky D, Bakkour A, Weintraub S, Mesulam MM, Caplan D, Dickerson BC (2010) Cortical neuroanatomic correlates of symptom severity in PPA. Neurology 75:358-366. PMCID: PMC2918888

Sapolsky D, Domoto-Reilly K, Dickerson BC (2014) Use of the Progressive Aphasia Severity Scale (PASS) in monitoring speech and language status in PPA. Aphasiology 28:993-1003. PMCID:PMC4235969

Perez DL, Dickerson BC, McGinnis SM, Sapolsky D, Johnson K, Searl M, Daffner KR (2013) You don't say: dynamic aphasia, another variant of PPA? J Alzheimers Dis 34:139-144. PMCID: PMC3621037

Dickerson BC (ed) (2015) Hodges' Frontotemporal Dementia, 2 Ed. Cambridge, UK: Cambridge Univ Press.

Complete List of Published Work in MyBibliography (>110 original scientific papers):



D. Research Support

Ongoing Research Support

P50 AG005134 (Hyman, PI) Role: Co-Investigator, Neuroimaging Subcore 04/01/2014 – 03/31/2019

Alzheimer’s Disease Research Center

R01 AG0323065 (Rosen, PI) Role: Co-investigator, Site PI 09/30/2009 – 08/31/2015

Frontotemporal Lobar Degeneration Neuroimaging Initiative

To establish multimodal markers of disease progression in FTLD (MRI, FDG-PET, blood, urine, CSF).

P01 AG036694 (P.I. Sperling) Role: Co-investigator 07/15/2010 – 06/30/2015

Impact of amyloid on the aging brain

To measure brain structure & function related to memory in older adults with or without brain amyloid.

R01 AG030311 (Barrett/Dickerson, MPI) 04/01/2012 - 3/31/2017

Neural mechanisms of affective salience in aging

To investigate changes in brain structure and function associated with age-related changes in affective reactivity and interoceptive sensitivity.

R21 NS077059 (Dickerson/Makris, MPI) 07/01/2012 - 06/30/2015

Large-scale language networks: Topography and selective degeneration

To better define the topography of language networks of the brain and measure whether the strength of connectivity is disrupted in and predicts progression in patients with primary progressive aphasia.

R21 MH097094 (Dickerson/Holt, MPI) 10/01/2012 - 09/30/2015

Social cognitive impairment in frontotemporal degeneration and schizophrenia

To investigate similarities and differences in the behavioral characteristics and neural substrates of social cognitive impairment in FTD and schizophrenia.

R01 EB014894 (Catana, PI) 1/1/2013 - 12/31/2016

MR-assisted PET data optimization for neuroimaging studies

Using an integrated MR-PET scanner, we will validate methods that benefit from simultaneous MR and PET data acquisition and explore the use of this new technology for applications focusing on Alzheimer’s disease.

R21 NS084156 (Dickerson, PI) 07/01/2013 - 06/30/2015

Pilot study of preclinical and prodromal frontotemporal degeneration

To identify MRI-based and psychophysiologic biomarkers of FTD and apply them to study the preclinical and prodromal course of FTD in members of families with autosomal dominant inherited FTD.

R21 NS079905 (Dickerson/Makris, MPI) 07/01/2013 - 07/31/2015

Imaging biomarkers of the FTD-ALS spectrum

To perform a preliminary study of the morphometry of gray matter nodes and white matter tracts in executive and motor networks and of the functional connectivity of these networks in FTD, ALS, and FTD-ALS.

Completed Research Support (last 3 years)

R01 NS062028 (Smith, PI) Role: Co-Investigator 08/01/2008 – 02/28/15 Small vessel disease and beta-amyloid deposition in mildly impaired cognition

IIRG-09-133560 (Dickerson, PI) 02/01/2010 - 01/31/2013

Alzheimer’s Association

Quantitative neuroanatomic biomarkers for dementia differential diagnosis

R01 AG029411 (Dickerson, PI) 09/15/2007 - 06/30/2012

Medial temporal lobe subregions in aging, MCI and AD: Structural and functional MRI

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