DPM-1001 decreased copper levels and ameliorated deficits in a mouse model of Wilson's disease
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چکیده
منابع مشابه
Cholinergic neuropathology in a mouse model of Alzheimer's disease
Transgenic mice over-expressing mutant human amyloid precursor protein (PDAPP mouse) develop several Alzheimer’s disease (AD)-like lesions including an age-related accumulation of amyloid-?-containing neuritic plaques. Although aged, heterozygous PDAPP mice also exhibit synaptic and glial cell changes, that is characteristic of AD pathology, no evidence of neurodegeneration has been observed. T...
متن کاملCholinergic neuropathology in a mouse model of Alzheimer's disease
Transgenic mice over-expressing mutant human amyloid precursor protein (PDAPP mouse) develop several Alzheimer’s disease (AD)-like lesions including an age-related accumulation of amyloid-?-containing neuritic plaques. Although aged, heterozygous PDAPP mice also exhibit synaptic and glial cell changes, that is characteristic of AD pathology, no evidence of neurodegeneration has been observed. T...
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The trace element copper is vital to the healthy functioning of organisms. Copper is used in a multitude of cellular activities including respiration, angiogenesis, and immune responses. Like other metals, copper homeostasis is a tightly regulated process. Copper is transported from dietary intake through the serum and into cells via a variety of transporters. There are a variety of copper chap...
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Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.
Cognitive impairment in Down syndrome (DS) is characterized by deficient learning and memory. Mouse genetic models of DS exhibit impaired cognition in hippocampally mediated behavioral tasks and reduced synaptic plasticity of hippocampal pathways. Enhanced efficiency of GABAergic neurotransmission was implicated in those changes. We have recently shown that signaling through postsynaptic GABA(B...
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ژورنال
عنوان ژورنال: Genes & Development
سال: 2018
ISSN: 0890-9369,1549-5477
DOI: 10.1101/gad.314658.118