β-Amyloid Modulation of Synaptic Transmission and Plasticity

2007111 citationsReviewbronze Open Access

Authors

Deepa V. Venkitaramani · Yale University

Jeannie Chin · University of California, San Francisco

William J. Netzer · Rockefeller University

Gunnar K. Gouras · Cornell University

Sylvain Lesné · University of Minnesota Medical Center

Roberto Malinow · Cold Spring Harbor Laboratory

Paul J. Lombroso

Abstract

The sequencing of β amyloid protein (Aβ) in 1984 led to the formulation of the “amyloid hypothesis” of Alzheimer's disease (AD) ([Glenner and Wong, 1984][1]). The hypothesis proposed that accumulation of Aβ is responsible for AD-related pathology, including Aβ deposits, neurofibrillary

Topics & Keywords

Alzheimer's disease research and treatments Neuroscience and Neuropharmacology Research Cellular transport and secretion

UN Sustainable Development Goals

Good health and well-being

Publication Details

Published in: Journal of Neuroscience

Volume 27, Issue 44, pp. 11832-11837

DOI: 10.1523/jneurosci.3478-07.2007

Field-Weighted Citation Impact: 6.67