Nature Communications (Nov 2017)
Neuronal hyperactivity due to loss of inhibitory tone in APOE4 mice lacking Alzheimer’s disease-like pathology
- Tal Nuriel,
- Sergio L. Angulo,
- Usman Khan,
- Archana Ashok,
- Qiuying Chen,
- Helen Y. Figueroa,
- Sheina Emrani,
- Li Liu,
- Mathieu Herman,
- Geoffrey Barrett,
- Valerie Savage,
- Luna Buitrago,
- Efrain Cepeda-Prado,
- Christine Fung,
- Eliana Goldberg,
- Steven S. Gross,
- S. Abid Hussaini,
- Herman Moreno,
- Scott A. Small,
- Karen E. Duff
Affiliations
- Tal Nuriel
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Sergio L. Angulo
- Department of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, The Robert F. Furchgott Center for Neural and Behavioral Science
- Usman Khan
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Archana Ashok
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Qiuying Chen
- Department of Pharmacology, Weill Cornell Medical College
- Helen Y. Figueroa
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Sheina Emrani
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Li Liu
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Mathieu Herman
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Geoffrey Barrett
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Valerie Savage
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Luna Buitrago
- Department of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, The Robert F. Furchgott Center for Neural and Behavioral Science
- Efrain Cepeda-Prado
- Department of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, The Robert F. Furchgott Center for Neural and Behavioral Science
- Christine Fung
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Eliana Goldberg
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Steven S. Gross
- Department of Pharmacology, Weill Cornell Medical College
- S. Abid Hussaini
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Herman Moreno
- Department of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, The Robert F. Furchgott Center for Neural and Behavioral Science
- Scott A. Small
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- Karen E. Duff
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University Medical Center
- DOI
- https://doi.org/10.1038/s41467-017-01444-0
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 14
Abstract
The APOE4 allele is the leading risk factor for late-onset Alzheimer’s disease, but how it might contribute to the disease is not clear. Here the authors show that a mouse expressing the human APOE4 allele displays hyperactivity in the entorhinal cortex due to a decreased inhibitory tone, which may in part explain accelerated Alzheimer’s pathology in APOE4 carriers.