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Synaptic retrogenesis and amyloid-beta in Alzheimer's disease.

Review article
Authors Pontus Wasling
Jonny Daborg
Ilse Riebe
My Andersson
Erik Portelius
Kaj Blennow
Eric Hanse
Henrik Zetterberg
Published in Journal of Alzheimer's disease : JAD
Volume 16
Issue 1
Pages 1-14
ISSN 1387-2877
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 1-14
Language en
Links dx.doi.org/10.3233/JAD-2009-0918
Keywords Alzheimer Disease, metabolism, pathology, Amyloid beta-Protein, metabolism, physiology, toxicity, Amyloid beta-Protein Precursor, metabolism, physiology, Animals, Brain, growth & development, Cell Proliferation, Glutamic Acid, physiology, Humans, Long-Term Potentiation, physiology, Memory, physiology, Neuronal Plasticity, physiology, Synapses, pathology, physiology
Subject categories Psychiatry

Abstract

Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings.

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