Nature Communications (Mar 2020)
Amyloid-β42/40 ratio drives tau pathology in 3D human neural cell culture models of Alzheimer’s disease
- Sang Su Kwak,
- Kevin J. Washicosky,
- Emma Brand,
- Djuna von Maydell,
- Jenna Aronson,
- Susan Kim,
- Diane E. Capen,
- Murat Cetinbas,
- Ruslan Sadreyev,
- Shen Ning,
- Enjana Bylykbashi,
- Weiming Xia,
- Steven L. Wagner,
- Se Hoon Choi,
- Rudolph E. Tanzi,
- Doo Yeon Kim
Affiliations
- Sang Su Kwak
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Kevin J. Washicosky
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Emma Brand
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Djuna von Maydell
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Jenna Aronson
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Susan Kim
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Diane E. Capen
- Center for Systems Biology and Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital, Harvard Medical School
- Murat Cetinbas
- Department of Molecular Biology, Massachusetts General Hospital
- Ruslan Sadreyev
- Department of Molecular Biology, Massachusetts General Hospital
- Shen Ning
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Enjana Bylykbashi
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Weiming Xia
- Geriatric Research Education and Clinical Center, Edith Nourse Rogers Memorial Veterans Hospital
- Steven L. Wagner
- Department of Neurosciences, University of California, San Diego
- Se Hoon Choi
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Rudolph E. Tanzi
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- Doo Yeon Kim
- Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, McCance Center for Brain Health, Massachusetts General Hospital, Harvard Medical School
- DOI
- https://doi.org/10.1038/s41467-020-15120-3
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 14
Abstract
The relationship between amyloid-β species and tau pathology in Alzheimer’s disease is not fully understood. Here, the authors show that it is the increased ratio of amyloid-β42 and 40 isoforms drives tau pathology in 3D human neural cell culture models of the disease.
