Abstract
Despite of long-standing evidence that beta-amyloid (Aβ) peptides have detrimental effects on synaptic function, the relationship between Aβ, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Aβ 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 Aβ accumulation on synaptic impairment and neuron loss and provides an overview of currently available AD mouse models showing these pathological alterations.
Highlights
AGING NEUROSCIENCEIntracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease
Alzheimer’s disease (AD) represents the most frequent form of dementia and is characterized by two major neuropathological hallmarks: (i) extracellular plaques composed of the 40–42 residues Aβ peptide (Hardy and Allsop, 1991) and (ii) neurofibrillary tangles, consisting of abnormal phosphorylated Tau protein (Braak and Braak, 1991)
We summarize the current achievements of modeling early intraneuronal Aβ accumulation in transgenic mice with their resulting pathological consequences
Summary
Intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease. Reviewed by: Asgar Zaheer, University of Iowa Hospitals and Clinics, USA H. K. Anandatheerthavarada, University of Pennsylvania, USA Salvatore Oddo, The University of Texas Health Science Center, USA P. Despite of long-standing evidence that beta-amyloid (Aβ) peptides have detrimental effects on synaptic function, the relationship between Aβ, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Aβ peptides is one of the key events leading to synaptic and neuronal dysfunction. The present review discusses the impact of intraneuronal Aβ accumulation on synaptic impairment and neuron loss and provides an overview of currently available AD mouse models showing these pathological alterations
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