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High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation
TLDR
It is concluded that Aβ is synaptotoxic even in the absence of plaques and that high levels of Aβ1–42 are insufficient to induce plaque formation in mice expressing wild-type hAPP, supporting the emerging view that plaque-independent Aβ toxicity plays an important role in the development of synaptic deficits in AD and related conditions. Expand
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
TLDR
Transgenic mice that express high levels of human mutant APP support a primary role for APP/Aβ in the genesis of AD and could provide a preclinical model for testing therapeutic drugs. Expand
Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease
TLDR
It is reported that hAPP mice have spontaneous nonconvulsive seizure activity in cortical and hippocampal networks, which is associated with GABAergic sprouting, enhanced synaptic inhibition, and synaptic plasticity deficits in the dentate gyrus. Expand
Amyloid-β–induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks
TLDR
Recent evidence that Aβ may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically is discussed. Expand
Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders.
TLDR
Results suggest that accumulation of wild-type alpha-synuclein may play a causal role in Parkinson's disease and related conditions. Expand
Alzheimer Mechanisms and Therapeutic Strategies
TLDR
Investigative and drug development efforts should be diversified to fully address the multifactoriality of Alzheimer's disease. Expand
Molecular profile of reactive astrocytes—Implications for their role in neurologic disease
TLDR
A summary of molecules whose levels of expression differentiate activated from resting astrocytes is provided and it becomes apparent that reactive astroCytes may benefit the injured nervous system by participating in diverse biological processes. Expand
Leukocyte Infiltration, Neuronal Degeneration, and Neurite Outgrowth after Ablation of Scar-Forming, Reactive Astrocytes in Adult Transgenic Mice
TLDR
These findings show that genetic targeting can be used to ablate scar-forming astrocytes and demonstrate roles for astroCytes in regulating leukocyte trafficking, repairing the BBB, protecting neurons, and restricting nerve fiber growth after injury in the adult central nervous system. Expand
Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model
TLDR
Reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high Aβ levels, and protected both transgenic and nontransgenic mice against excitotoxicity. Expand
Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models.
TLDR
It is shown that overexpression of FAD(717V-->F)-mutant human APP in neurons of transgenic mice decreases the density of presynaptic terminals and neurons well before these mice develop amyloid plaques, suggesting a neurotoxic effect of Abeta that is independent of plaque formation. Expand
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