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. 2010 Mar 10:2:8.
doi: 10.3389/fnagi.2010.00008. eCollection 2010.

Intracellular accumulation of amyloid-Beta - a predictor for synaptic dysfunction and neuron loss in Alzheimer's disease

Thomas A Bayer  1 , Oliver Wirths
Affiliations

Intracellular accumulation of amyloid-Beta - a predictor for synaptic dysfunction and neuron loss in Alzheimer's disease

Thomas A Bayer et al. Front Aging Neurosci. .

Abstract

Despite of long-standing evidence that beta-amyloid (Abeta) peptides have detrimental effects on synaptic function, the relationship between Abeta, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Abeta peptides is one of the key events leading to synaptic and neuronal dysfunction. Many studies have been carried out using transgenic mouse models of Alzheimer's disease (AD) which have been proven to be valuable model systems in modern AD research. The present review discusses the impact of intraneuronal Abeta accumulation on synaptic impairment and neuron loss and provides an overview of currently available AD mouse models showing these pathological alterations.

Keywords: alzheimer; amyloid; intraneuronal Aβ; neuron loss; oligomers; synaptic dysfunction; transgenic mice.

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Figures

Figure 1
Figure 1
Intraneuronal Aβ accumulation and impaired LTP in APP/PS1KI mice. Schematic drawing of the hippocampus (A). At 6 months of age deficits in synaptic transmission in the form of altered LTP are detected in APP/PS1KI mice (B–D). Intraneuronal accumulation of Aβ peptides occurs already at 2 months of age in the CA1 region of the hippocampus (E) and precedes neuron loss which becomes evident at 6 months of age (F,G).
See this image and copyright information in PMC

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