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transgenic-mice
9 studies tagged transgenic-mice, dated 1996-12-01 to 2013-01-01. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Changes of the enteric nervous system in amyloid-β protein precursor transgenic mice correlate with disease progression 2013-01-01
- Environmental enrichment prevents astroglial pathological changes in the hippocampus of APP transgenic mice, model of Alzheimer's disease 2012-09-28
- The Psen1-L166P-knock-in mutation leads to amyloid deposition in human wild-type amyloid precursor protein YAC transgenic mice 2012-03-29
Studies
9 studies carry this tag.
Date range
1996 to 2013
Top journals
- Experimental neurology 2
- Journal of Alzheimer's disease : JAD 2
- Brain research 1
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1
- Neurobiology of aging 1
7 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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In Alzheimer's disease (AD), fatal neuronal cell loss occurs long before relevant evidence can lead to a reliable diagnosis.
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Alzheimer's disease (AD) is a neurodegenerative disease that affects neurons and glial cells and leads to dementia.
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Genetically engineered mice have been generated to model cerebral β-amyloidosis, one of the hallmarks of Alzheimer disease (AD) pathology, based on the overexpression of a mutated cDNA of the amyloid-β precursor protein (AβPP) or by knock-in of the murine Aβpp gene alone or with presenilin1 mutations.
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36/100
Chronic cerebral ischemia may accelerate clinicopathological changes in Alzheimer's disease.
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Synaptic changes occur early in the course of Alzheimer's disease and are key to understanding the initial events in associated neurodegenerative processes.
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Inflammation has been argued to play a primary role in the pathogenesis of Alzheimer's disease (AD).
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Previous studies of Abeta-induced neuronal damage of hippocampal cells in culture have provided strong evidence that deregulation of the Cdk5/p35 kinase system is involved in the neurodegeneration pathway.
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Proteases and their inhibitors play key roles in physiological and pathological processes.
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Alzheimer's disease is characterized by the extracellular deposition of beta-amyloid peptide (Abeta) in cerebral plaques and evidence is accumulating that amyloid is neurotoxic.