A5015418396- Iron Metabolism and Disorders
- Hemoglobinopathies and Related Disorders
- Trace Elements in Health
- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Pharmacological Effects and Toxicity Studies
- Extracellular vesicles in disease
- Neurological diseases and metabolism
- Mitochondrial Function and Pathology
- DNA Repair Mechanisms
- ATP Synthase and ATPases Research
- Neurogenesis and neuroplasticity mechanisms
- Restless Legs Syndrome Research
- Anesthesia and Neurotoxicity Research
- Neuroscience and Neuropharmacology Research
Penn State Milton S. Hershey Medical Center
2022-2023
Pennsylvania State University
2022-2023
National Institute on Aging
2019-2021
National Institutes of Health
2019
University of New Haven
2019
Iron is essential for normal brain development and function. Hence, understanding the mechanisms of iron efflux at blood-brain barrier their regulation are critical establishment homeostasis. Here, we have investigated role exosomes in mediating transfer H-ferritin (FTH1)- or transferrin (Tf)-bound across endothelial cells (BBBECs). Our study used ECs derived from human-induced pluripotent stem that grown bicameral chambers. When were exposed to 55Fe-Tf 55Fe-FTH1, 55Fe activity exosome...
Abstract Background Apo- (iron free) and holo- bound) transferrin (Tf) participate in precise regulation of brain iron uptake at endothelial cells the blood–brain barrier. Apo-Tf indicates an iron-deficient environment stimulates release, while holo-Tf sufficient suppresses additional release. Free is exported through ferroportin, with hephaestin as aid to process. Until now, molecular mechanisms apo- influence on release was largely unknown. Methods Here we use a variety cell culture...
Alzheimer's disease (AD) has several hallmark features including amyloid-β (Aβ) plaque deposits and neuronal loss. Here, we characterized Aβ aggregation parvalbumin-positive (PV) GABAergic neurons in 6-9-month-old 5xFAD mice harboring mutations associated with familial AD. We used immunofluorescence staining to compare three regions the frontal cortex-prelimbic (PrL), cingulate (Cg, Cg1 Cg2), secondary motor (M2) cortices-along primary somatosensory (S1) cortex. quantified density of...
The brain requires iron for a number of processes, including energy production. Inadequate or excessive amounts can be detrimental and lead to neurological disorders. As such, regulation uptake is required proper functioning. Understanding both the movement into how this process regulated crucial address dysfunctions with in disease successfully use transferrin receptor system drug delivery.Using vivo steady state infusions apo- holo-transferrin lateral ventricle, we demonstrate regulatory...
A bstract Excessive brain iron accumulation is observed early in the onset of Alzheimer's disease, notably prior to widespread proteinopathy. These findings suggest that increases levels are due a dysregulation transport mechanism at blood–brain barrier. Astrocytes release signals (apo‐ and holo‐transferrin) communicate needs endothelial cells order modulate transport. Here we use iPSC‐derived astrocytes investigate how early‐disease amyloid‐β disrupt secreted by stimulate from cells. We...
Excessive brain iron accumulation is observed in early the onset of Alzheimer's disease, notably prior to widespread proteinopathy. These findings suggest that increases levels are due a dysregulation transport mechanism at blood-brain barrier. Astrocytes release signals (apo- and holo-transferrin) communicate needs endothelial cells order modulate transport. Here we use iPSC-derived astrocytes investigate how early-disease amyloid-β disrupt secreted by stimulate from cells. We demonstrate...
Abstract Adequate and timely delivery of iron is essential for brain development. The uptake transferrin‐bound (Tf) into the peaks at time myelination, whereas recently discovered H‐ferritin (FTH1) transport continues to increase beyond peak in myelination. Here, we interrogate impact dietary deficiency (ID) on FTH1‐ Tf‐bound iron. In present study, used C57BL/6J male female mice a developing (post‐natal day (PND) 15) adult age (PND 85). mice, ID results increased from both FTH1 Tf males...
Abstract Background : Apo- (iron free) and holo- bound) transferrin (Tf) participate in precise regulation of brain iron uptake at endothelial cells the blood-brain barrier. Apo-Tf indicates an deficient environment stimulates release, while holo-Tf sufficient suppresses additional release. Free is exported through ferroportin, with hephaestin as aid to process. Until now, molecular mechanism apo- holo-Tf’s influence on release was largely unknown. Methods Here we use a variety cell culture...
Apo- (iron free) and holo- bound) transferrin (Tf) participate in precise regulation of brain iron uptake at endothelial cells the blood-brain barrier. Apo-Tf indicates an deficient environment stimulates release, while holo-Tf sufficient suppresses additional release. Free is exported through ferroportin, with hephaestin as aid to process. Until now, molecular mechanism apo- holo-Tf's influence on release was largely unknown.
Abstract Background : The brain requires iron for a number of processes, including energy production. Inadequate or excessive amounts can be detrimental and lead to neurological disorders. As such, regulation uptake is required proper functioning. Understanding both the movement into how this process regulated crucial address dysfunctions with in disease successfully use transferrin receptor system drug delivery. Methods Using vivo steady state infusions apo- holo-transferrin lateral...