Transgenic mice overexpressing amyloid precursor protein exhibit early metabolic deficits and a pathologically low leptin state associated with hypothalamic dysfunction in arcuate neuropeptide Y neurons.
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Overview
publication date
- January 1, 2014
published in
has subject area
- Adiposity
- Alzheimer Disease
- Amyloid beta-Peptides
- Amyloid beta-Protein Precursor
- Animals
- Arcuate Nucleus of Hypothalamus
- Brain
- Brain Chemistry
- Disease Models, Animal
- Disease Progression
- Fasting
- Feeding Behavior
- Female
- Genes, Reporter
- Humans
- Hypothalamus
- Leptin
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Transgenic
- Mutation
- Neurons
- Neuropeptide Y
- Patch-Clamp Techniques
- Plaque, Amyloid
- Weight Loss