No hippocampal neuron or synaptic bouton loss in learning-impaired aged β-Amyloid precursor protein-null mice

@article{Phinney1999NoHN,
  title={No hippocampal neuron or synaptic bouton loss in learning-impaired aged $\beta$-Amyloid precursor protein-null mice},
  author={Amie L. Phinney and Michael E. Calhoun and David P. Wolfer and H. P. Lipp and H. Zheng and Mathias Jucker},
  journal={Neuroscience},
  year={1999},
  volume={90},
  pages={1207-1216}
}
Lack of APP and APLP2 in GABAergic Forebrain Neurons Impairs Synaptic Plasticity and Cognition.
TLDR
It is shown that APP is also widely expressed in several interneuron subtypes, both in hippocampus and cortex, and a crucial role of APP family proteins in inhibitory interneurons to maintain functional network activity is revealed.
Functional consequences of the lack of amyloid precursor protein in the mouse dentate gyrus in vivo
TLDR
It is suggested that the deletion of APP may affect presynaptic plasticity of synaptic transmission at the perforant path–granule cell synapse but leaves synaptic efficacy intact and LTP preserved, possibly due to functional redundancy within the APP gene family.
Impaired theta-gamma coupling in APP-deficient mice
TLDR
Lack of APP reduces oscillatory coupling in LFP recordings from specific brain regions, despite not affecting the amplitude of the oscillations, and reveals reduced cross-frequency coupling as a functional marker of APP deficiency at the network level.
Spatial relationship between synapse loss and β‐amyloid deposition in Tg2576 mice
TLDR
The results provide the first quantitative morphological evidence at the ultrastructure level of a spatial relationship between β‐amyloid plaques and synapse loss within the hippocampus and the entorhinal cortex of Tg2576 mice.
Cerebral Amyloid Induces Aberrant Axonal Sprouting and Ectopic Terminal Formation in Amyloid Precursor Protein Transgenic Mice
TLDR
Cerebral amyloid deposition has neurotropic effects and is the main cause of aberrant sprouting in AD brain; the magnitude and significance of sprouted in AD have been underestimated; and cerebral amyloids leads to the disruption of neuronal connectivity which, in turn, may significantly contribute to AD dementia.
Deletion of the amyloid precursor‐like protein 1 (APLP1) enhances excitatory synaptic transmission, reduces network inhibition but does not impair synaptic plasticity in the mouse dentate gyrus
TLDR
It is concluded that APLP1 deficiency on its own does not lead to defects in synaptic plasticity, but affects synaptic transmission and network inhibition in the dentate gyrus.
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