We are analyzing https://link.springer.com/article/10.1007/s00406-013-0449-5.

Title:
Pathology of clinical and preclinical Alzheimer’s disease | European Archives of Psychiatry and Clinical Neuroscience
Description:
Alzheimer’s disease (AD) is characterized neuropathologically by the presence of amyloid plaques, neuritic plaques, and neurofibrillary tangles (NFTs). These lesions occur not only in demented individuals with AD but also in non-demented persons. In non-demented individuals, amyloid and neuritic plaques are usually accompanied with NFTs and are considered to represent asymptomatic or preclinical AD (pre-AD) pathology. Here, we defined and characterized neuropathological differences between clinical AD, non-demented pre-AD, and non-AD control cases. Our results show that clinical AD may be defined as cases exhibiting late stages of NFT, amyloid, and neuritic plaque pathology. This is in contrast to the neuropathological changes characteristic of pre-AD, which display early stages of these lesions. Both AD and pre-AD cases often exhibit cerebral amyloid angiopathy (CAA) and granulovacuolar degeneration (GVD), and when they do, these AD-related pathologies were at early stages in pre-AD cases and at late stages in symptomatic AD. Importantly, NFTs, GVD, and CAA were also observed in non-AD cases, i.e., in cases without amyloid plaque pathology. Moreover, soluble and dispersible, high-molecular-weight amyloid β-protein (Aβ) aggregates detected by blue-native polyacrylamide gel electrophoresis were elevated in clinical AD compared to that in pre-AD and non-AD cases. Detection of NFTs, GVD, and CAA in cases without amyloid plaques, presently classified as non-AD, is consistent with the idea that NFTs, GVD, and CAA may precede amyloid plaque pathology and may represent a pre-amyloid plaque stage of pre-AD not yet considered in the current recommendations for the neuropathological diagnosis of AD. Our finding of early stages of AD-related NFT, amyloid, and GVD pathology provides a more clear definition of pre-AD cases that is in contrast to the changes in clinical AD, which is characterized by late stages of these AD-related pathologies. The observed elevation of soluble/dispersible Aβ aggregates from pre-AD compared to that in AD cases suggests that, in addition to more widespread AD-related pathologies, soluble/dispersible Aβ aggregates in the neuropil play a role in the conversion of pre-AD to clinical AD.
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Keywords {🔍}

article, google, scholar, pubmed, alzheimers, cas, disease, amyloid, pathology, neuropathol, thal, braak, clinical, cases, pread, stages, protein, research, brain, acta, plaques, neurofibrillary, tau, tangles, plaque, granulovacuolar, degeneration, del, tredici, neurobiol, alzheimer, neurol, oligomers, yamaguchi, cerebral, angiopathy, soluble, access, study, aging, usa, privacy, cookies, content, griffin, attems, nfts, gvd, aggregates, neurology,

Topics {✒️}

high-molecular-weight amyloid β-protein high-molecular weight aβ-oligomers n-methyl-d-aspartate receptors inhibit long-term potentiation dietmar rudolf thal month download article/chapter pre-amyloid plaque stage sds-page induces dimerization escrt-iii subunit chmp2b article european archives soluble/dispersible aβ aggregates widespread ad-related pathologies cerebral amyloid angiopathy long-term depression full article pdf amyloid plaque pathology privacy choices/manage cookies cerebrovascular amyloid protein amyloid precursor protein neurodegenerative diseases christine von arnim received research support article thal european economic area unfolded protein response shankar gm abeta-protein deposition clinical neuroscience aims neuritic plaque pathology app23 mice correlates post-mortem correlates related immunohistochemical markers author information authors abeta immunotherapy leads predominant aβ-species dunhill medical trust ad-related pathologies alzheimer neurofibrillary tangles dendritic tree morphology de felice fg dickson dw progressive motor disturbance mice expressing mutant jack cr jr capetillo-zarate chronic stress response distinct apoe epsilon4 rat dentate gyrus scientific advisory board masters cl

Questions {❓}

Watt AD, Perez KA, Rembach A, Sherrat NA, Hung LW, Johanssen T, McLean CA, Kok WM, Hutton CA, Fodero-Tavoletti M, Masters CL, Villemagne VL, Barnham KJ (2013) Oligomers, fact or artefact?

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         description: Alzheimer’s disease (AD) is characterized neuropathologically by the presence of amyloid plaques, neuritic plaques, and neurofibrillary tangles (NFTs). These lesions occur not only in demented individuals with AD but also in non-demented persons. In non-demented individuals, amyloid and neuritic plaques are usually accompanied with NFTs and are considered to represent asymptomatic or preclinical AD (pre-AD) pathology. Here, we defined and characterized neuropathological differences between clinical AD, non-demented pre-AD, and non-AD control cases. Our results show that clinical AD may be defined as cases exhibiting late stages of NFT, amyloid, and neuritic plaque pathology. This is in contrast to the neuropathological changes characteristic of pre-AD, which display early stages of these lesions. Both AD and pre-AD cases often exhibit cerebral amyloid angiopathy (CAA) and granulovacuolar degeneration (GVD), and when they do, these AD-related pathologies were at early stages in pre-AD cases and at late stages in symptomatic AD. Importantly, NFTs, GVD, and CAA were also observed in non-AD cases, i.e., in cases without amyloid plaque pathology. Moreover, soluble and dispersible, high-molecular-weight amyloid β-protein (Aβ) aggregates detected by blue-native polyacrylamide gel electrophoresis were elevated in clinical AD compared to that in pre-AD and non-AD cases. Detection of NFTs, GVD, and CAA in cases without amyloid plaques, presently classified as non-AD, is consistent with the idea that NFTs, GVD, and CAA may precede amyloid plaque pathology and may represent a pre-amyloid plaque stage of pre-AD not yet considered in the current recommendations for the neuropathological diagnosis of AD. Our finding of early stages of AD-related NFT, amyloid, and GVD pathology provides a more clear definition of pre-AD cases that is in contrast to the changes in clinical AD, which is characterized by late stages of these AD-related pathologies. The observed elevation of soluble/dispersible Aβ aggregates from pre-AD compared to that in AD cases suggests that, in addition to more widespread AD-related pathologies, soluble/dispersible Aβ aggregates in the neuropil play a role in the conversion of pre-AD to clinical AD.
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