BIOGRAPHICAL SKETCH
NAME
POSITION TITLE
Associate Professor of Neurology,
Bradford C. Dickerson, M.D., M.MSc.
Harvard Medical School
eRA COMMONS USER NAME (credential, e.g.,
agency login)
EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as
BCDICKERSON
nursing, and include postdoctoral training.)
DEGR
INSTITUTION AND LOCATION
EE
YEAR(s)
FIELD OF STUDY
Southern Methodist University, Dallas, TX
Univ. of Illinois at Chicago College Of Medicine
Brigham & Women’s Hospital, Boston, MA
Massachusetts General & Brigham & Women's
Hospitals
Harvard-Martinos
Center for Biomedical Imaging, MGH
B.S.
M.D.
Harvard-Brigham Behavioral Neurology Unit
Harvard Medical School/MIT, Boston, MA
1990
1994-1999
1999-2000
2000-2003
2003-2005
2003-2005
M.Sc.
2003-2005
Biomedical Engineering
Medicine
Internship, Medicine
Residency, Neurology
Fellowship,
Neuroimaging
Fellowship, Cognitive
and Behavioral
Clinical
Investigation
Neurology
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 CoDirector 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
2003Assistant in Neurology, Massachusetts General Hospital, Boston, MA
2003-2006
Instructor in Neurology, Harvard Medical School, Boston, MA
2005Co-Director, Neuroimaging Group, MGH Gerontology Research Unit, Charlestown, MA
2005Director of Clinical Applications, MGH Morphometry Analysis Center, Charlestown, MA
2006-2008
Assistant Professor of Neurology, Harvard Medical School, Boston, MA
2007Co-Director, Imaging Subcore, MGH Alzheimer’s Disease Research Center
2008Director, MGH Frontotemporal Dementia Unit
2008Associate Professor of Neurology, Harvard Medical School
2009Co-Director, MGH Center for Neural Systems Investigations (CNSi)
2013Rickles Endowed Chair in PPA/FTD Research, Massachusetts General Hospital, Boston, MA
2015Director, MGH Center for Translational Brain Mapping, Boston, MA
Other Experience and Professional Memberships
1995Society for Neuroscience
2001American Academy of Neurology; Organization for Human Brain Mapping
2004200420042005200520072008-
200920092010201020122015Honors
1995
1995-99
1996
1997
1998
1999
2001
2002
2005
2013
2014
Greater Boston Alzheimer’s Association Medical & Scientific Advisory Board
Member, grant review committees, multiple private foundations, including Fidelity Research
Foundation, Alzheimer’s Association, Association for FTD
Member, Society for Behavioral and Cognitive Neurology
Member, grant review committees, multiple federal agencies, including National Science
Foundation, NAME NIH Study Section, NIH Challenge Grant Review Panel #10 ZRG1 BDA-A
Founding Chair, Charles River Association for Memory (with Dan Schacter, Howard
Eichenbaum, John Gabrieli; we have held biannual meetings of 80-100 attendees )
Editorial Board member, Hippocampus, Frontiers in Neuroscience, Neurodegenerative Disease
Management, The Open Neurology Journal, Neuroimage: Clinical
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
Faculty Member, Harvard FAS Mind/Brain/Behavior committee
Director, Primer of Behavioral Neurology Annual CME Course, American Academy of Neurology
Co-Director, Ånnual Harvard Dementia CME Course
Member, Association for Frontotemporal Dementia Medical Advisory Board
Chair, External Advisory Committee, Conte Center Grant P50 MH 094263, Prefrontal and
Medial-Temporal Interactions in Memory, PI Howard Eichenbaum
Associate Editor, Behavioral Neurology Section, Cortex
Walter Rice Craig Summer Research Fellowship, Univ. of Illinois at Urbana-Champaign
James Scholar, UIC College of Medicine
Honorable Mention, UIC College of Medicine Student Research Symposium
Second place, Sigma Xi Session of Rush University Research Forum
Alpha Omega Alpha
David M. Olkon Honors Scholarship, UIC College of Medicine
Outstanding Resident Teacher in Neurology, Harvard Medical School
Partners in Excellence Award (Neurology Chief Residents), Partners Healthcare System
Mentor of the Year Award, Partners Neurology Residents
Norman Geschwind Award in Behavioral Neurology, American Academy of Neurology
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-4, 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, DetoledoMorrell 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 (http://www.ppaconnection.org), 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):
http://www.ncbi.nlm.nih.gov/sites/myncbi/bradford.dickerson.1/bibliography/40752539/public/?sort=date&directi
on=ascending
D. Research Support
Ongoing Research Support
P50 AG005134 (Hyman, PI) Role: Co-Investigator, Neuroimaging Subcore
Alzheimer’s Disease Research Center
04/01/2014 – 03/31/2019
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
Small vessel disease and beta-amyloid deposition in mildly impaired cognition
08/01/2008 – 02/28/15
IIRG-09-133560 (Dickerson, PI)
Alzheimer’s Association
Quantitative neuroanatomic biomarkers for dementia differential diagnosis
02/01/2010 - 01/31/2013
R01 AG029411 (Dickerson, PI)
09/15/2007 - 06/30/2012
Medial temporal lobe subregions in aging, MCI and AD: Structural and functional MRI