Abstract
This commentary reviews the role of the Alzheimer amyloid peptide Aβ on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Aβ4-42. Aβ4-42 is highly abundant in the brain of Alzheimer’s disease (AD) patients. It demonstrates increased neurotoxicity compared to full length Aβ, suggesting an important role in the pathogenesis of AD. Transgenic Tg4-42 mice, a model for sporadic AD, express human Aβ4-42 in Cornu Ammonis (CA1) neurons, and develop age-dependent hippocampal neuron loss and neurological deficits. In contrast to other transgenic AD mouse models, the Tg4-42 model exhibits synaptic hyperexcitability, altered synaptic short-term plasticity with no alterations in short- and long-term potentiation. The outcomes of this study are discussed in comparison with controversial results from other AD mouse models.
Highlights
Center (UMG), Georg-August-University, von-Siebold-Strasse 5, 37075 Göttingen, Germany; Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), Humboldtallee 23, Center for Physiology and Pathophysiology, Institute for Neuro- and Sense Physiology, University Medical
Inslices order studytothe possible chronic neurotoxic effects of N-truncated tissue weretosubjected three different test paradigms, i.e., input–output curves, Aβ4-42 on synaptic function and plasticity orthodromically evoked field potentials were recorded in hippocampal slices
The acute hippocampal tissue slices were subjected to three different test paradigms, i.e., input–output curves, paired-pulse facilitation (PPF), as well as recording for short-term (PTP, Short-term potentiation (STP)) and long-term potentiation (LTP)
Summary
It is generally well accepted that Alzheimer’s disease (AD) is neuropathologically characterized by extracellular beta-amyloid plaques (Aβ) and neurofibrillary tangles. Without to plaque formation and[14], appearance of neurofibrillary tangles Both models were analyzed with athat pan-Aβ antibody in order to visualize intraneuronal. Aβ and compared the Aβ pathology to 5XFAD mice [14], a widely used mouse model with typical amyloid plaque deposits in CA1 neurons of the hippocampus of 3-month-old transgenic mice. Alzheimer’s disease (AD) mouse model with intraneuronal detected in CA1 in Tg4-42 mice (A–C), but not in 5XFAD (D–F), whereas plaques were only found in. Immunohistochemistry was performed on 4 μm paraffin secondary anti-rabbit and anti-mouse antibodies (1:200) were purchased from DAKO (Glostrup, Denmark). Staining was visualized using the ABC method, with a Vectastain kit
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