Salvador Borges-Neto

Overview:

Expertise:

1. Diagnostic and Prognostic Utility of Cardiovascular Nuclear Medicine in  Heart Disease.
2. The Role of Cardiac PET/CT  in Cardiac Sarcoidosis and Ischemic Heart Disease.
3. The Role of Nuclear Cardiology in Diagnosis and Management of Amyloidosis.
4. Left Ventricular Dyssynchrony Evaluation by GSPECT.

I am a Professor of Radiology (Nuclear Medicine) and Internal Medicine at Duke University Medical Center. I also serve as the Medical Director of Nuclear Cardiology at Duke Health System with Duke Heart Center. I received my medical doctorate from the Federal Fluminense University in Brazil. I subsequently completed a Cardiology Fellowship at Antonio Pedro University Hospital in Brazil and a second Fellowship in the Medicine/Cardiovascular division at Brigham and Women's Hospital in Boston. I continued my education with a fellowship in Nuclear Cardiology at the Methodist Hospital Baylor College of Medicine in Houston, Texas and finally in Nuclear Medicine in the Department of Radiology at Duke University Medical Center. I have lectured extensively internationally and have published 130+ publications in peer reviewed scientific professional journals. I am a founding member of the American Society of Nuclear Cardiology, Fellow of the American College of Cardiology, Fellow of the American College of Nuclear Medicine and Fellow of the American Heart Association. My clinical and Research interests include the role of cardiac imaging in predicting outcomes and guiding therapy. I have developed one of the largest Nuclear Cardiology Data Bases in the US. More recently my primarily research interest also includes the use of New Radiopharmaceuticals for the Diagnosis and Treatment of Oncologic Diseases (Theranostics). I have led a Team for the implementation of Diagnosis and Treatment of Neuroendocrine Tumors which became a Center of Reference for this Disease Diagnosis and Treatment with PRRT. serving as the PI for Expanded Access for Therapeutic Use of 177-Lu-DOTAO-Tyr3-Octreotide (Advanced Accelerator Applications SA – AAA) –Compationate Use – “177 Lu-Dotatate for Midgut Neuroendocrine Tumors and 177 Lu-Dotatate for GPENET’. Clinical Trials.Gov. 

Positions:

Professor of Radiology

Radiology, Nuclear Medicine
School of Medicine

Professor of Medicine

Medicine, Cardiology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1981

Federal University of Fluminense (Brazil)

Intern in Medicine

Federal University of Fluminense (Brazil)

Clinical Fellowship

Federal University of Fluminense (Brazil)

Research Fellowship

Harvard University

Research Fellowship

Baylor College of Medicine

Research Fellowship

Duke University School of Medicine

Nuclear Medicine Residency

Duke University School of Medicine

Grants:

Impact of Disclosing Amyloid Imaging Results to Cognitively Normal Individuals

Administered By
Psychiatry & Behavioral Sciences, Geriatric Behavioral Health
Awarded By
Brigham and Women's Hospital
Role
Investigator
Start Date
End Date

Defining Myocardial Viability & Infarction:Contrast MRI

Administered By
Medicine, Cardiology
Awarded By
National Institutes of Health
Role
Consultant
Start Date
End Date

Lutathera Compassionate Use Expanded Access StudyNeoFIND - [68Ga]-NeoBOMB1 imaging in patients with malignancies known to overexpress GRPR

Administered By
Radiology, Nuclear Medicine
Awarded By
Advanced Accelerator Applications SA
Role
Principal Investigator
Start Date
End Date

Publications:

Genome-wide association analysis of hippocampal volume identifies enrichment of neurogenesis-related pathways.

Adult neurogenesis occurs in the dentate gyrus of the hippocampus during adulthood and contributes to sustaining the hippocampal formation. To investigate whether neurogenesis-related pathways are associated with hippocampal volume, we performed gene-set enrichment analysis using summary statistics from a large-scale genome-wide association study (N = 13,163) of hippocampal volume from the Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) Consortium and two year hippocampal volume changes from baseline in cognitively normal individuals from Alzheimer's Disease Neuroimaging Initiative Cohort (ADNI). Gene-set enrichment analysis of hippocampal volume identified 44 significantly enriched biological pathways (FDR corrected p-value < 0.05), of which 38 pathways were related to neurogenesis-related processes including neurogenesis, generation of new neurons, neuronal development, and neuronal migration and differentiation. For genes highly represented in the significantly enriched neurogenesis-related pathways, gene-based association analysis identified TESC, ACVR1, MSRB3, and DPP4 as significantly associated with hippocampal volume. Furthermore, co-expression network-based functional analysis of gene expression data in the hippocampal subfields, CA1 and CA3, from 32 normal controls showed that distinct co-expression modules were mostly enriched in neurogenesis related pathways. Our results suggest that neurogenesis-related pathways may be enriched for hippocampal volume and that hippocampal volume may serve as a potential phenotype for the investigation of human adult neurogenesis.
Authors
Horgusluoglu-Moloch, E; Risacher, SL; Crane, PK; Hibar, D; Thompson, PM; Saykin, AJ; Nho, K; Alzheimer’s Disease Neuroimaging Initiative (ADNI),
MLA Citation
Horgusluoglu-Moloch, Emrin, et al. “Genome-wide association analysis of hippocampal volume identifies enrichment of neurogenesis-related pathways.Sci Rep, vol. 9, no. 1, Oct. 2019, p. 14498. Pubmed, doi:10.1038/s41598-019-50507-3.
URI
https://scholars.duke.edu/individual/pub1417787
PMID
31601890
Source
pubmed
Published In
Scientific Reports
Volume
9
Published Date
Start Page
14498
DOI
10.1038/s41598-019-50507-3

Utility of diastolic dyssynchrony in the setting of cardiac resynchronization therapy.

Authors
Fudim, M; Borges-Neto, S
MLA Citation
Fudim, Marat, and Salvador Borges-Neto. “Utility of diastolic dyssynchrony in the setting of cardiac resynchronization therapy.J Nucl Cardiol, Sept. 2019. Pubmed, doi:10.1007/s12350-019-01889-4.
URI
https://scholars.duke.edu/individual/pub1409779
PMID
31512196
Source
pubmed
Published In
J Nucl Cardiol
Published Date
DOI
10.1007/s12350-019-01889-4

Molecular Imaging and Therapy for Neuroendocrine Tumors.

OPINION STATEMENT: Neuroendocrine tumors (NETs) are relatively rare, with 12,000-15,000 new cases diagnosed annually in the USA. Although NETs are a diverse group of neoplasms, they share common molecular targets that can be exploited using nuclear medicine techniques for both imaging and therapy. NETs have traditionally been imaged with SPECT imaging using 111In-labeled octreotide analogs to detect neoplasms with somatostatin receptors. In addition, certain NETs (pheochromocytomas, paragangliomas, and neuroblastomas) are also effectively imaged using 123I- or 131I-labeled metaiodobenzylguanidine (MIBG), an analog of guanethidine. More recently, PET imaging with 68Ga-labeled somatostatin receptor (SSR) analogs allows neuroendocrine tumors to be imaged with much higher sensitivity. 68Ga-DOTATATE was approved as a PET tracer by the FDA in June 2016. In addition to imaging, both MIBG and DOTATATE can be labeled with therapeutic radionuclides to deliver targeted radiation selectively to macroscopic and microscopic tumor sites. The incorporation of the same molecular probe for imaging and therapy provides a radio-theranostic approach to identifying, targeting, and treating tumors. Over the years, several centers have experience treating NETs with high-dose 131I-MIBG. 177Lu-DOTATATE was approved by the FDA in 2018 for treatment of gastroenteropancreatic NETs and constitutes a major advancement in the treatment of these diseases. In this paper, we provide an overview of imaging and treating neuroendocrine tumors using MIBG and SSR probes. Although uncommon, neuroendocrine tumors have provided the largest experience for targeted radionuclide imaging and therapy (with the exception of radioiodine treatment for thyroid disease). In addition to benefitting patients with these rare tumors, the knowledge gained provides a blueprint for the development of future paired diagnostic/therapeutic probes for treating other diseases, such as prostate cancer.
Authors
MLA Citation
Desai, Hemant, et al. “Molecular Imaging and Therapy for Neuroendocrine Tumors.Curr Treat Options Oncol, vol. 20, no. 10, Aug. 2019, p. 78. Pubmed, doi:10.1007/s11864-019-0678-6.
URI
https://scholars.duke.edu/individual/pub1406491
PMID
31468190
Source
pubmed
Published In
Current Treatment Options in Oncology
Volume
20
Published Date
Start Page
78
DOI
10.1007/s11864-019-0678-6

The prognostic value of diastolic and systolic mechanical left ventricular dyssynchrony among patients with coronary artery disease and heart failure.

BACKGROUND: Prevalence and prognostic value of diastolic and systolic dyssynchrony in patients with coronary artery disease (CAD) + heart failure (HF) or CAD alone are not well understood. METHODS: We included patients with gated single-photon emission computed tomography (GSPECT) myocardial perfusion imaging (MPI) between 2003 and 2009. Patients had at least one major epicardial obstruction ≥ 50%. We assessed the association between dyssynchrony and outcomes, including all-cause and cardiovascular death. RESULTS: Of the 1294 patients, HF was present in 25%. Median follow-up was 6.7 years (IQR 4.9-9.3) years with 537 recorded deaths. Patients with CAD + HF had a higher incidence of dyssynchrony than patients with CAD alone (diastolic BW 28.8% for the HF + CAD vs 14.7% for the CAD alone). Patients with CAD + HF had a lower survival than CAD alone at 10 years (33%; 95% CI 27-40 vs 59; 95% CI 55-62, P < 0.0001). With one exception, HF was found to have no statistically significant interaction with dyssynchrony measures in unadjusted and adjusted survival models. CONCLUSIONS: Patients with CAD + HF have a high prevalence of mechanical dyssynchrony as measured by GSPECT MPI, and a higher mortality than CAD alone. However, clinical outcomes associated with mechanical dyssynchrony did not differ in patients with and without HF.
Authors
Fudim, M; Fathallah, M; Shaw, LK; James, O; Samad, Z; Piccini, JP; Hess, PL; Borges-Neto, S
MLA Citation
URI
https://scholars.duke.edu/individual/pub1404124
PMID
31392509
Source
pubmed
Published In
J Nucl Cardiol
Published Date
DOI
10.1007/s12350-019-01843-4

Translating Alzheimer's disease-associated polymorphisms into functional candidates: a survey of IGAP genes and SNPs.

The International Genomics of Alzheimer's Project (IGAP) is a consortium for characterizing the genetic landscape of Alzheimer's disease (AD). The identified and/or confirmed 19 single-nucleotide polymorphisms (SNPs) associated with AD are located on non-coding DNA regions, and their functional impacts on AD are as yet poorly understood. We evaluated the roles of the IGAP SNPs by integrating data from many resources, based on whether the IGAP SNP was (1) a proxy for a coding SNP or (2) associated with altered mRNA transcript levels. For (1), we confirmed that 12 AD-associated coding common SNPs and five nonsynonymous rare variants are in linkage disequilibrium with the IGAP SNPs. For (2), the IGAP SNPs in CELF1 and MS4A6A were associated with expression of their neighboring genes, MYBPC3 and MS4A6A, respectively, in blood. The IGAP SNP in DSG2 was an expression quantitative trait loci (eQTL) for DLGAP1 and NETO1 in the human frontal cortex. The IGAP SNPs in ABCA7, CD2AP, and CD33 each acted as eQTL for AD-associated genes in brain. Our approach for identifying proxies and examining eQTL highlighted potentially impactful, novel gene regulatory phenomena pertinent to the AD phenotype.
Authors
Katsumata, Y; Nelson, PT; Estus, S; Alzheimer's Disease Neuroimaging Initiative (ADNI),; Fardo, DW
MLA Citation
Katsumata, Yuriko, et al. “Translating Alzheimer's disease-associated polymorphisms into functional candidates: a survey of IGAP genes and SNPs.Neurobiol Aging, vol. 74, Feb. 2019, pp. 135–46. Pubmed, doi:10.1016/j.neurobiolaging.2018.10.017.
URI
https://scholars.duke.edu/individual/pub1366883
PMID
30448613
Source
pubmed
Published In
Neurobiol Aging
Volume
74
Published Date
Start Page
135
End Page
146
DOI
10.1016/j.neurobiolaging.2018.10.017