Analysis Tools
nervous system
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• microglia are seen associated with compact plaques
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• mice develop two types of amyloid plaques beginning at 9 months of age, either compact, typically round (compact) plaque which are seen at early stages or fluffy amyloid beta material (diffuse) plaque which are seen at later stages
(J:102542)
• at 12 months of age, plaques are seen in the frontal, parietal, occipital, cingulate, and temporal cortices, in the hippocampus, and in the white matter, most often in the corpus callosum
(J:102542)
• at 18 months, amyloid beta deposits develop in the entorhinal and piriform cortices such that 21 months, density is high in the piriform cortex but relatively low in the entorhinal cortex
(J:102542)
• at 18 months, plaques spread to extracortical sites, mainly to the striatum and septum and at 21 months, they are seen in the colliculi (thalamus, amygdala, olfactory bulb, and olfactory nucleus but not in the cerebellum, pons, or medulla oblongata
(J:102542)
• mice develop vascular amylod-beta deposits in leptomeningeal vessels and their larger intracortical branches at 12 months of age
(J:102542)
• however, mice do not develop neurofibrillary tangles or show signs of neurodegeneration
(J:102542)
• amyloid plaques are detected in the brains of these mutant transgenic mice but not in Apptm1Ck transgenic or Apptm1Ck Tg(PDGFB-PSEN1M146L)2Jhd transgenic mutant mice up to 20 months of age
(J:102879)
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• activated astrocytes are seen associated with plaques
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• mice develop abnormal cholinergic fiber aggregates and enlarged terminals after 12 months of age
(J:102542)
• in 1-year old animals, a relatively high number of cholinergic fiber aggregates in the cortex are observed in transgenic; at 20 months of age, a few such areas of densed cholinergic fiber aggregations are observed in other APP-targeted mice
(J:102879)
• cholinergic fibers of large diameter are seen in layer 1 of the entorhinal cortex in mutant transgenic mice more prominently than in the other strains, but such fibers are present even in controls
(J:102879)
• clusters of ballooned and spherical acetylcholine-immunoreactive terminals are observed in the periphery of compact amyloid plaques around the amyloid core in 12-month old animals, and numbers increase with age and plaque load
(J:102879)
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homeostasis/metabolism
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• mice develop two types of amyloid plaques beginning at 9 months of age, either compact, typically round (compact) plaque which are seen at early stages or fluffy amyloid beta material (diffuse) plaque which are seen at later stages
(J:102542)
• at 12 months of age, plaques are seen in the frontal, parietal, occipital, cingulate, and temporal cortices, in the hippocampus, and in the white matter, most often in the corpus callosum
(J:102542)
• at 18 months, amyloid beta deposits develop in the entorhinal and piriform cortices such that 21 months, density is high in the piriform cortex but relatively low in the entorhinal cortex
(J:102542)
• at 18 months, plaques spread to extracortical sites, mainly to the striatum and septum and at 21 months, they are seen in the colliculi (thalamus, amygdala, olfactory bulb, and olfactory nucleus but not in the cerebellum, pons, or medulla oblongata
(J:102542)
• mice develop vascular amylod-beta deposits in leptomeningeal vessels and their larger intracortical branches at 12 months of age
(J:102542)
• however, mice do not develop neurofibrillary tangles or show signs of neurodegeneration
(J:102542)
• amyloid plaques are detected in the brains of these mutant transgenic mice but not in Apptm1Ck transgenic or Apptm1Ck Tg(PDGFB-PSEN1M146L)2Jhd transgenic mutant mice up to 20 months of age
(J:102879)
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hematopoietic system
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• microglia are seen associated with compact plaques
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immune system
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• microglia are seen associated with compact plaques
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