John M. Wells
Boston University
31 Papers
301 Citations
John M. Wells is an academic researcher from Boston University. The author has contributed to research in topics: Apolipoprotein E & Amyloid precursor protein. The author has an hindex of 20, co-authored 31 publications. Previous affiliations of John M. Wells include Veterans Health Administration & Edith Nourse Rogers Memorial Veterans Hospital.
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Papers
APOE, vascular pathology, and the AD brain.
Agustin G. Yip,Ann C. McKee,Roger C. Green,John M. Wells,H. Young,L. A. Cupples,Lindsay A. Farrer +6 more
TL;DR: A role for ε4 in some of the microvascular changes commonly found in AD and are consistent with a potential amyloidogenic role forε4 are suggested.
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.
Identification of the protein disulfide isomerase family member PDIp in experimental Parkinson's disease and Lewy body pathology
Kelly J. Conn,Wenwu Gao,Wenwu Gao,Ann C. McKee,Ann C. McKee,Michael S. Lan,M. David Ullman,M. David Ullman,Patricia B. Eisenhauer,Patricia B. Eisenhauer,Patricia B. Eisenhauer,Richard E. Fine,Richard E. Fine,John M. Wells,John M. Wells +14 more
TL;DR: Findings suggest that increased PDIp expression in dopaminergic (DA) neurons might contribute to LB formation and neurodegeneration, and that this increased PDip expression may be the result of proteasome impairment.
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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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Allele epsilon 4 of apolipoprotein E shows a dose effect on age at onset of Pick disease.
Lindsay A. Farrer,Carmela R. Abraham,Ladislav Volicer,Elizabeth J. Foley,Neil W. Kowall,Ann C. McKee,John M. Wells +6 more
TL;DR: The dose effect of the ϵ4 allele on age at onset of dementias other than AD and the association of ApoE immunoreactivity with neurons and Pick bodies support a broader role for ApOE in the pathogenesis of neuronal degeneration through interactions with the neuronal cytoskeleton.
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