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Journal ArticleDOI

Conformational change as one of the earliest alterations of tau in Alzheimer’s disease

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TLDR
It is suggested that the formation of the MCI epitope is one of the earliest pathological alterations of tau in AD.
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This article is published in Neurobiology of Aging.The article was published on 2000-09-01. It has received 297 citations till now. The article focuses on the topics: Neurofibrillary tangle & Tau protein.

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Neuropathological Alterations in Alzheimer Disease

TL;DR: Postmortem studies have enabled the staging of the progression of both amyloid and tangle pathologies, and the development of diagnostic criteria that are now used worldwide, and these cross-sectional neuropathological data have been largely validated by longitudinal in vivo studies using modern imaging biomarkers such as amyloids PET and volumetric MRI.
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Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury.

TL;DR: This work reviews 48 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 professionalathletes, 1 football player and 2 boxers.
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Trans-Synaptic Spread of Tau Pathology In Vivo

TL;DR: The mouse recapitulates the tauopathy that defines the early stages of AD and provides a model for testing mechanisms and functional outcomes associated with disease progression and support a trans-synaptic mechanism of spread along anatomically connected networks, between connected and vulnerable neurons.
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Aβ Immunotherapy Leads to Clearance of Early, but Not Late, Hyperphosphorylated Tau Aggregates via the Proteasome

TL;DR: It is shown that Abeta immunotherapy reduces not only extracellular Abeta plaques but also intracellular AbETA accumulation and most notably leads to the clearance of early tau pathology.
References
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Journal ArticleDOI

Neuropathological stageing of Alzheimer-related changes.

Heiko Braak, +1 more
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
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Abnormal tau phosphorylation at Ser396 in Alzheimer's disease recapitulates development and contributes to reduced microtubule binding.

TL;DR: It is demonstrated that native A68 does not bind to microtubules (MTs), yet dephosphorylated A68 regains the ability to bind to MTs, and phosphorylation of Ser396 may destabilize MTs in AD, resulting in the degeneration of affected cells.
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Staging of Alzheimer-Related Cortical Destruction

TL;DR: The patterns of staining typically found with each of these techniques in the brains of patients with progressively severe AD are described and how the specific changes observed can be used as a staging system for diagnostic purposes are described.
Journal ArticleDOI

Tau protein and the neurofibrillary pathology of Alzheimer's disease.

TL;DR: Current evidence suggests that protein kinases or protein phosphatases with a specificity for serine/threonine-proline residues are involved in the abnormal phosphorylation of tau.
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Biopsy-derived adult human brain tau is phosphorylated at many of the same sites as Alzheimer's disease paired helical filament tau

TL;DR: Examination of human adult tau from brain biopsies demonstrated that biopsy-derived tau is phosphorylated at most sites thought to be abnormally phosphorylate tau, suggesting that the down-regulation of phosphatases in the AD brain could lead to the generation of maximallyosphorylated PHF-tau that does not bind microtubules and aggregates as PHFs in neurofibrillary tangles and dystrophic neurites.
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