G
Geoffry L. Curran
Researcher at Mayo Clinic
Publications - 67
Citations - 3271
Geoffry L. Curran is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Blood–brain barrier & Amyloid beta. The author has an hindex of 34, co-authored 63 publications receiving 2964 citations. Previous affiliations of Geoffry L. Curran include Rosalind Franklin University of Medicine and Science & University of Rochester.
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Journal ArticleDOI
An autoradiographic evaluation of AV-1451 Tau PET in dementia.
Val J. Lowe,Geoffry L. Curran,Ping Fang,Amanda M. Liesinger,Keith A. Josephs,Joseph E. Parisi,Kejal Kantarci,Bradley F. Boeve,Mukesh K. Pandey,Tyler J. Bruinsma,David S. Knopman,David T.W. Jones,Leonard Petrucelli,Casey Cook,Neill R. Graff-Radford,Dennis W. Dickson,Ronald C. Petersen,Clifford R. Jack,Melissa E. Murray +18 more
TL;DR: Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV- fourteen51 binding and suggests complexity in AV- 1451 binding.
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Transplanted Senescent Cells Induce an Osteoarthritis-Like Condition in Mice
Ming Xu,Elizabeth W. Bradley,Megan M. Weivoda,Soyun M. Hwang,Tamar Pirtskhalava,Teresa Decklever,Geoffry L. Curran,Mikolaj Ogrodnik,Diana Jurk,Kurt O. Johnson,Val J. Lowe,Tamar Tchkonia,Jennifer J. Westendorf,James L. Kirkland +13 more
TL;DR: A novel senescent cell transplantation model involving injection of small numbers of senescent or nonsenescent cells from the ear cartilage of luciferase-expressing mice into the knee joint area of wild-type mice is presented, showing that senescent cells can induce an OA-like state.
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Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats.
Bartolome Burguera,Marta E. Couce,Geoffry L. Curran,Michael D. Jensen,Ricardo V. Lloyd,Margot P. Cleary,Joseph F. Poduslo +6 more
TL;DR: Findings strongly suggest that the leptin receptor (OB-R) in the BBB can be easily saturated and explain the defect in leptin transport into the brain described in this study.
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β-sheet breaker peptide inhibitor of Alzheimer's amyloidogenesis with increased blood–brain barrier permeability and resistance to proteolytic degradation in plasma
TL;DR: Because of its five- to sevenfold increase in permeability at the BBB and its resistance to proteolysis in the plasma, this polyamine-modified beta-sheet breaker peptide may prove to be an effective inhibitor of amyloidogenesis in vivo and, hence, an important therapy for Alzheimer's disease.
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Polyamine modification increases the permeability of proteins at the blood-nerve and blood-brain barriers.
TL;DR: Although cationic proteins are known to interact with fixed anionic charges on the lumen of the microvascular endothelium, this observation of decreased permeability with increased positive charge distribution along the aliphatic carbon chain of the polyamines implies mechanisms other than simple electrostatic interaction involving charge density.