Rachel D. Hendrix
Postdoctoral Fellow
Also affiliated: Northern Arizona University (2013); Washington University in St. Louis (2020–2024); University of Arkansas Medical Center (2017); Hope Center for Neurological Disorders (2020–2024)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Rachel D. Hendrix investigates the mechanisms underlying Alzheimer's disease, with a focus on the role of amyloid-beta peptides and their impact on cellular processes. Her work has explored how amyloid precursor protein influences insulin-degrading enzyme levels and how amyloid-beta disrupts glucose transporter localization in astrocytes, potentially affecting brain and blood glucose levels. Hendrix has also examined the potential of pharmacological interventions, such as pimavanserin, to suppress Alzheimer's pathology in mouse models. Her research further extends to the timing of biomarker changes in relation to symptom onset in sporadic Alzheimer's disease and the use of CSF biomarkers to predict cognitive impairment risk in the elderly. Hendrix has published 16 papers, with an h-index of 8 and 282 citations, and collaborates with researchers at the University of Arkansas for Medical Sciences.
Metrics
- h-index: 8
- Publications: 13
- Citations: 281
Positions
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Postdoctoral Fellow 2018–presentWashington University in St. Louis School of Medicine Neurology ORCID
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Postdoctoral Fellow publications 2017–2025University of Arkansas for Medical Sciences ORCID
Selected Publications
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Isotretinoin Use During Consolidation in Acute Promyelocytic Leukemia Following Standard All-Trans Retinoic Acid (ATRA)-Based Induction: A Case Report (2026)
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Navigating Hyperhemolysis in Sickle Cell Disease: Insights from Literature (2025)
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Intranasal Corticosteroid Use and Risk of Invasive Fungal Sinusitis in Acute Myeloid Leukemia, Myelodysplastic Syndrome and Post Transplant Patients (2024)
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Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues (2018)
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Functional assessments through novel proteomics approaches: Application to insulin/IGF signaling in neurodegenerative disease' (2018)
Collaboration Network
Top Collaborators
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Functional assessments through novel proteomics approaches: Application to insulin/IGF signaling in neurodegenerative disease'
- Intranasal Corticosteroid Use and Risk of Invasive Fungal Sinusitis in Acute Myeloid Leukemia, Myelodysplastic Syndrome and Post Transplant Patients
- Isotretinoin Use During Consolidation in Acute Promyelocytic Leukemia Following Standard All-Trans Retinoic Acid (ATRA)-Based Induction: A Case Report
- Navigating Hyperhemolysis in Sickle Cell Disease: Insights from Literature
- Navigating Hyperhemolysis in Sickle Cell Disease: Insights from Literature
- Functional assessments through novel proteomics approaches: Application to insulin/IGF signaling in neurodegenerative disease'
- Functional assessments through novel proteomics approaches: Application to insulin/IGF signaling in neurodegenerative disease'
- Functional assessments through novel proteomics approaches: Application to insulin/IGF signaling in neurodegenerative disease'
- Functional assessments through novel proteomics approaches: Application to insulin/IGF signaling in neurodegenerative disease'
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
- Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues
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