S
Suzana Petanceska
Researcher at Nathan Kline Institute for Psychiatric Research
Publications - 39
Citations - 3465
Suzana Petanceska is an academic researcher from Nathan Kline Institute for Psychiatric Research. The author has contributed to research in topics: Amyloid precursor protein & Amyloid. The author has an hindex of 26, co-authored 38 publications receiving 3321 citations. Previous affiliations of Suzana Petanceska include New York University & National Institutes of Health.
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Journal ArticleDOI
A Cholesterol-Lowering Drug Reduces β-Amyloid Pathology in a Transgenic Mouse Model of Alzheimer's Disease
Lorenzo M. Refolo,Miguel A. Pappolla,John LaFrancois,Brian Malester,Stephen D. Schmidt,T. Thomas-Bryant,G. S. Tint,Rong Wang,Marc Mercken,Suzana Petanceska,Karen Duff +10 more
TL;DR: It is demonstrated that hypocholesterolemia is associated with reduced Abeta accumulation suggesting that lowering cholesterol by pharmacological means may be an effective approach for reducing the risk of developing AD.
Journal ArticleDOI
Aβ localization in abnormal endosomes: association with earliest Aβ elevations in AD and Down syndrome
Anne M. Cataldo,Anne M. Cataldo,Suzana Petanceska,Nicole B. Terio,Corrinne M. Peterhoff,Robert A. Durham,Marc Mercken,Pankaj D. Mehta,Joseph D. Buxbaum,Vahram Haroutunian,Ralph A. Nixon,Ralph A. Nixon +11 more
TL;DR: These studies support growing evidence that endosomal pathology contributes significantly to Abeta overproduction and accumulation in sporadic AD and in AD associated with DS and may signify earlier disease-relevant disturbances of the signaling functions of endosomes.
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Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology
Miguel A. Pappolla,Tara Bryant-Thomas,Donald Herbert,Javier Pacheco,M. Fabra Garcia,M. Manjon,Xavier Gironès,Tracey L. Henry,Etsuro Matsubara,Daniel Zambón,Benjamin Wolozin,Mary Sano,Félix F. Cruz-Sánchez,Leon J. Thal,Suzana Petanceska,Lorenzo M. Refolo +15 more
TL;DR: Serum hypercholesterolemia may be an early risk factor for the development of AD amyloid pathology.
Journal ArticleDOI
App Gene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome
Anne M. Cataldo,Suzana Petanceska,Corrinne M. Peterhoff,Nicole B. Terio,Charles J. Epstein,Angela Villar,Elaine J. Carlson,Matthias Staufenbiel,Ralph A. Nixon +8 more
TL;DR: It is shown that a genetic model of DS (trisomy 21), the segmental trisomy 16 mouse Ts65Dn, develops enlarged neuronal early endosomes, increased immunoreactivity for markers of endosome fusion, and endosomal recycling similar to those in AD and DS individuals.
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Ovariectomy and 17β-estradiol modulate the levels of Alzheimer’s amyloid β peptides in brain
TL;DR: The finding that E2 treatment is associated with diminution of brain Aβ levels suggests that modulation of Aβ metabolism may be one of the ways by which estrogen replacement therapy prevents or delays the onset of AD or both in postmenopausal women.