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Peter J. Morin
Researcher at Boston University
Publications - 27
Citations - 1379
Peter J. Morin is an academic researcher from Boston University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 12, co-authored 22 publications receiving 1169 citations. Previous affiliations of Peter J. Morin include United States Department of Veterans Affairs & Edith Nourse Rogers Memorial Veterans Hospital.
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Journal ArticleDOI
TDP-43 Proteinopathy and Motor Neuron Disease in Chronic Traumatic Encephalopathy
Ann C. McKee,Brandon E. Gavett,Robert S. Stern,Christopher J. Nowinski,Robert C. Cantu,Neil W. Kowall,Daniel P. Perl,E. Tessa Hedley-Whyte,Bruce H. Price,Christopher P. Sullivan,Peter J. Morin,H. J. Lee,Caroline A. Kubilus,Daniel H. Daneshvar,Megan Wulff,Andrew E. Budson +15 more
TL;DR: This work has found the first pathological evidence that repetitive head trauma experienced in collision sports might be associated with the development of a motor neuron disease.
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Three Dimensional Human Neuro-Spheroid Model of Alzheimer's Disease Based on Differentiated Induced Pluripotent Stem Cells.
Han-Kyu Lee,Han-Kyu Lee,Clara Velazquez Sanchez,Clara Velazquez Sanchez,Mei Chen,Mei Chen,Peter J. Morin,John M. Wells,Eugene B. Hanlon,Weiming Xia,Weiming Xia +10 more
TL;DR: The results demonstrate that the iPSC-differentiated 3D human neuro-spheroid model can be a physiologically relevant and valid model for testing efficacy of AD drug.
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Amyloid Precursor Protein Is Synthesized by Retinal Ganglion Cells, Rapidly Transported to the Optic Nerve Plasma Membrane and Nerve Terminals, and Metabolized
Peter J. Morin,Carmela R. Abraham,Anil Amaratunga,Robin J. Johnson,Glenn Huber,Julie H. Sandell,Richard E. Fine +6 more
TL;DR: Investigation of the synthesis, axonal transport, and processing of the β‐amyloid precursor protein (APP) in in vivo rabbit retinal ganglion cells finds a protease(s) that can potentially cleave APP to generate an amyloidogenic fragment is present in the same optic nerve membrane compartment as APP.
Journal ArticleDOI
Retromer disruption promotes amyloidogenic app processing
Christopher P. Sullivan,Anthony G. Jay,Edward C. Stack,Maria Pakaluk,Erin Wadlinger,Richard E. Fine,John M. Wells,Peter J. Morin +7 more
TL;DR: Reduced retromer activity can mimic the effects of familial AD Presenilin mutations on APP processing and promote export of amyloidogenic APP derivatives.
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Amyloid β synaptotoxicity is Wnt-PCP dependent and blocked by fasudil
Katherine J. Sellers,Christina Elliott,Joshua Jackson,Anshua Ghosh,Elena M. Ribe,Ana I. Rojo,Heledd H. Jarosz-Griffiths,Iain A. Watson,Weiming Xia,Mikhail V. Semenov,Peter J. Morin,Nigel M. Hooper,Rod Porter,Jane E. Preston,Raya Al-Shawi,George S. Baillie,Simon Lovestone,Antonio Cuadrado,Michael K. Harte,Paul Simons,Deepak Srivastava,Richard Killick +21 more
TL;DR: This work has demonstrated that Aβ induces Dickkopf‐1 (Dkk1), which in turn activates the Wnt–planar cell polarity (Wnt‐PCP) pathway to drive tau pathology and neuronal death.