Samantha Katz

ORCID: 0000-0001-6048-7605
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About
Contact & Profiles
Research Areas
  • Dementia and Cognitive Impairment Research
  • Alzheimer's disease research and treatments
  • Radiopharmaceutical Chemistry and Applications
  • Monoclonal and Polyclonal Antibodies Research
  • Lanthanide and Transition Metal Complexes
  • Advanced Neuroimaging Techniques and Applications
  • HER2/EGFR in Cancer Research
  • Medical Imaging Techniques and Applications
  • Parkinson's Disease Mechanisms and Treatments
  • Health, Environment, Cognitive Aging
  • Cholinesterase and Neurodegenerative Diseases
  • Chronic Lymphocytic Leukemia Research
  • Neurology and Historical Studies
  • Research on Leishmaniasis Studies
  • Protein purification and stability
  • Immunodeficiency and Autoimmune Disorders
  • Trauma Management and Diagnosis
  • Neurological and metabolic disorders
  • Shoulder and Clavicle Injuries
  • Advanced MRI Techniques and Applications
  • Synthesis and Biological Evaluation
  • Ophthalmology and Eye Disorders
  • Cerebrospinal fluid and hydrocephalus
  • Glioma Diagnosis and Treatment
  • Anatomy and Medical Technology

Yale Cancer Center
2024

Yale University
2022-2024

Massachusetts General Hospital
2004-2023

Gordon Center for Medical Imaging
2019-2023

Harvard University
2019-2023

Maastricht University
2021

Athinoula A. Martinos Center for Biomedical Imaging
2021

Cliniques Universitaires Saint-Luc
2021

Florey Institute of Neuroscience and Mental Health
2021

The University of Melbourne
2021

Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology longitudinal studies normal aging and dementia, including assessment the central model Alzheimer's disease (AD) pathogenesis, according to which TAU begins focally but expands catastrophically under influence amyloid-β (Aβ) mediate neurodegeneration cognitive decline. Initial deposition occurs many years before Aβ a specific area medial temporal lobe. Building on recent work that focus...

10.1126/scitranslmed.abc0655 article EN Science Translational Medicine 2021-01-20

Neuroimaging studies of autosomal dominant Alzheimer's disease (ADAD) enable characterization the trajectories cerebral amyloid-β (Aβ) and tau accumulation in decades prior to clinical symptom onset. Longitudinal rates regional measured with positron emission tomography (PET) their relationship other biomarker cognitive changes remain be fully characterized ADAD.Fourteen ADAD mutation carriers (Presenilin-1 E280A) 15 age-matched non-carriers from Colombian kindred underwent 2-3 sessions Aβ...

10.1186/s13195-020-00765-5 article EN cc-by Alzheimer s Research & Therapy 2021-01-15

The aim of this study was to evaluate the efficacy tamoxifen in vivo experimental models cutaneous (CL) and visceral leishmaniasis (VL) caused by Leishmania braziliensis chagasi, respectively.Drug activity assessed against intracellular amastigotes treating infected macrophage cultures evaluating number cells. In tested L. braziliensis-infected BALB/c mice chagasi-infected hamsters. Treatment with 20 mg/kg/day administered for 15 days intraperitoneal route. Efficacy evaluated through...

10.1093/jac/dkn509 article EN Journal of Antimicrobial Chemotherapy 2008-11-19

To develop imaging biomarkers of diseases in the Lewy body spectrum and to validate these markers against postmortem neuropathologic findings.Four cognitively normal participants with Parkinson disease (PD), 4 PD cognitive impairments, 10 dementia bodies underwent amyloid [11C]Pittsburgh compound B (PiB) dopamine transporter (DAT) [11C]Altropane. All 18 had annual neurologic examinations. developed impairment before death. Neuropathologic examinations assessed scored Braak bodies, Thal...

10.1212/wnl.0000000000007855 article EN Neurology 2019-06-27

To compare how structural MRI, fluorodeoxyglucose (FDG), and flortaucipir (FTP) PET signals predict cognitive decline in high-amyloid vs low-amyloid participants with the goal of determining which biomarker combination would result highest increase statistical power for prevention trials.In this prospective cohort study, we analyzed data from clinically normal adults Harvard Aging Brain Study FDG, FTP, Pittsburgh compound B (PiB)-PET acquired within a year evaluations over mean 3-year...

10.1212/wnl.0000000000012108 article EN Neurology 2021-05-07

Regional cortical thinning in dementia with Lewy bodies (DLB) and Parkinson disease (PDD) may underlie some aspect of their clinical impairments; atrophy likely reflects extensive body pathology alpha-synuclein deposits, as well associated Alzheimer's co-pathologies, when present. Here we investigated the topographic distribution these diseases compared to cognitively normal PD healthy non-PD control subjects, explored association regional features evaluated impact amyloid deposition....

10.1016/j.nicl.2020.102196 article EN cc-by-nc-nd NeuroImage Clinical 2020-01-01

(1) Purpose: The glycoprotein non-metastatic melanoma B (gpNMB) is a type 1 transmembrane protein that overexpressed in numerous cancers, including triple-negative breast cancer (TNBC). Its overexpression associated with lower overall survival of patients TNBC. Tyrosine kinase inhibitors such as dasatinib can upregulate gpNMB expression, which has the potential to enhance therapeutic targeting anti-gpNMB antibody drug conjugates glembatumumab vedotin (CDX-011). Our primary aim quantify...

10.3390/cancers15051589 article EN Cancers 2023-03-03

We previously reported that asymptomatic Presenilin-1 (PSEN1) mutation carriers have elevated tau levels in entorhinal cortex their late 30s, an average of six years before estimated clinical onset (Quiroz et al., 2018). Here we build on these results using anatomically-defined rhinal region, hypothesized to be the initial site cortical deposition non-demented individuals genetically-determined develop Alzheimer's disease mid-forties (median age 44 +/- 2 years). Forty family members (age...

10.1016/j.jalz.2018.06.2282 article EN Alzheimer s & Dementia 2018-07-01

We previously reported that asymptomatic Presenilin-1 (PSEN1) mutation carriers have elevated tau levels in entorhinal cortex their late 30s, an average of six years before estimated clinical onset (Quiroz et al., 2018). Here we build on these results using anatomically-defined rhinal region, hypothesized to be the initial site cortical deposition non-demented individuals genetically-determined develop Alzheimer's disease mid-forties (median age 44 ± 2 years). Forty family members (age...

10.1016/j.jalz.2018.06.1145 article EN Alzheimer s & Dementia 2018-07-01

Purpose: To evaluate safety and efficacy of Antegren™ (natalizumab), a humanized monoclonal IgG4 antibody to ?4 integrin, in randomized, double-blind, placebo-controlled, multicenter study patients with active Crohn's disease (CD) receiving infliximab (IFX). Methods: Patients aged ≥18 years CD despite ongoing IFX treatment (Crohn's Disease Activity Index [CDAI] score ≥150) were randomized 2:1 receive natalizumab (300 mg; n = 52) or placebo (n 27) every 4 weeks for total 3 infusions. received...

10.14309/00000434-200410001-00785 article EN The American Journal of Gastroenterology 2004-10-01

In the Colombian kindred with autosomal dominant Alzheimer's disease (AD), Presenilin-1 (PSEN1) E280A carriers develop AD dementia by age 49 near 100% certainty. this ongoing study, we aim to assess longitudinal PET measures in their ability track changes tau and beta-amyloid (Aβ) pathology along trajectory from preclinical clinical stages. We analyzed data 15 participants Kindred: 8 mutation (age: 37.3±6.2 [28-45]), 7 age-matched non-carriers 38.4±6.1 [28-45]). All underwent two sessions of...

10.1016/j.jalz.2019.06.3982 article EN Alzheimer s & Dementia 2019-07-01

Amyloid deposition is common in the Lewy body dementias (LBD), dementia with bodies (DLB) and Parkinson (PDD), can be detected amyloid imaging. We previously showed that cortical thinning on structural MRI specific regions affected AD (“AD signature”) detect pathology, even amyloid-positive asymptomatic subjects. However, contribution of pathology to regional LBD remains unclear. hypothesized topography would similar DLB PDD but more severe DLB, overlapping signature basis accumulation,...

10.1016/j.jalz.2019.06.4910 article EN Alzheimer s & Dementia 2019-07-01

Amyloid deposition is common in the Lewy body dementias (LBD), dementia with bodies (DLB) and Parkinson (PDD), can be detected amyloid imaging. We previously showed that cortical thinning on structural MRI specific regions affected AD ("AD signature") detect pathology, even amyloid-positive asymptomatic subjects. However, contribution of pathology to regional LBD remains unclear. hypothesized topography would similar DLB PDD but more severe DLB, overlapping signature basis accumulation,...

10.1016/j.jalz.2019.06.914 article EN Alzheimer s & Dementia 2019-07-01

Abstract Purpose To quantify the degree and identify timeframe of glycoprotein nonmetastatic melanoma B (gpNMB) upregulation in vivo after treatment with Src tyrosine kinase inhibitor, dasatinib, by longitudinal PET imaging 89 Zr-labeled anti-gpNMB antibody ([ Zr]Zr-DFO-CR011). The goal is to timepoint at which administer corresponding drug conjugate, CDX-011 following dasatinib enhance therapeutic efficacy sequential targeted treatments using noninvasive guide therapy. Methods First, TNBC...

10.21203/rs.3.rs-2223276/v1 preprint EN cc-by Research Square (Research Square) 2022-11-14
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