PMC:6582309 / 5664-7241
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/6582309","sourcedb":"PMC","sourceid":"6582309","source_url":"https://www.ncbi.nlm.nih.gov/pmc/6582309","text":"Protein aggregation is an established pathogenic mechanism in AD, although little is known about the initiation of this process in vivo. As human brain research largely depends on the results of postmortem studies, an insight into the early stages of the disease, when protein aggregates are most likely to occur, is difficult. Novel and better animal models would therefore be very helpful to study the progress of AD in humans. The clinical course of the disease in humans could be monitored by brain imaging (CT, MRI). The exact connection between protein aggregates, such as extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles (NFTs), the latter composed of hyperphosphorylated microtubule associated protein (TAU), in the brains of patients with AD, and neurodegeneration is therefore still unknown. It does seem that the AD is caused by the accumulation of amyloid plaques and neurofibrillary fibers, although this is not absolutely confirmed and generally accepted (Medeiros et al., 2011). Stronger evidence that aggregates do trigger neurodegeneration (the so-called amyloid hypothesis) and are not just a consequence of the neurodegeneration, is provided by mutations in the gene for the amyloid beta precursor protein (APP) present in some human patients with AD (Selkoe, 1991; Hardy and Higgins, 1992; Hardy and Selkoe, 2002; Lansbury and Lashuel, 2006). Similarly, amyloid plaques are present in different brain regions in dogs with CCD clinical symptoms, and they can be present even before clinical signs of this disease become obvious.","tracks":[{"project":"2_test","denotations":[{"id":"31249505-20553310-38601476","span":{"begin":1017,"end":1021},"obj":"20553310"},{"id":"31249505-1673054-38601477","span":{"begin":1309,"end":1313},"obj":"1673054"},{"id":"31249505-1566067-38601478","span":{"begin":1334,"end":1338},"obj":"1566067"},{"id":"31249505-12130773-38601479","span":{"begin":1358,"end":1362},"obj":"12130773"},{"id":"31249505-17051203-38601480","span":{"begin":1386,"end":1390},"obj":"17051203"}],"attributes":[{"subj":"31249505-20553310-38601476","pred":"source","obj":"2_test"},{"subj":"31249505-1673054-38601477","pred":"source","obj":"2_test"},{"subj":"31249505-1566067-38601478","pred":"source","obj":"2_test"},{"subj":"31249505-12130773-38601479","pred":"source","obj":"2_test"},{"subj":"31249505-17051203-38601480","pred":"source","obj":"2_test"}]},{"project":"0_colil","denotations":[{"id":"31249505-20553310-736901","span":{"begin":1017,"end":1021},"obj":"20553310"},{"id":"31249505-1673054-736902","span":{"begin":1309,"end":1313},"obj":"1673054"},{"id":"31249505-1566067-736903","span":{"begin":1334,"end":1338},"obj":"1566067"},{"id":"31249505-12130773-736904","span":{"begin":1358,"end":1362},"obj":"12130773"},{"id":"31249505-17051203-736905","span":{"begin":1386,"end":1390},"obj":"17051203"}],"attributes":[{"subj":"31249505-20553310-736901","pred":"source","obj":"0_colil"},{"subj":"31249505-1673054-736902","pred":"source","obj":"0_colil"},{"subj":"31249505-1566067-736903","pred":"source","obj":"0_colil"},{"subj":"31249505-12130773-736904","pred":"source","obj":"0_colil"},{"subj":"31249505-17051203-736905","pred":"source","obj":"0_colil"}]}],"config":{"attribute types":[{"pred":"source","value type":"selection","values":[{"id":"2_test","color":"#c4ec93","default":true},{"id":"0_colil","color":"#ec93de"}]}]}}