Tau pathology in children and young adults: can you still be unconditionally baptist?

Duyckaerts, Charles

doi:10.1007/s00401-010-0794-7

Cited by 63 publications

(41 citation statements)

References 16 publications

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“…One of the main results at baseline is that only 28% of subjects with a mean age of 76 years were amyloid positive, a feature that is slightly below the picture of the main on-going multicentre studies [45][46][47][48][49] .…”

Section: Discussionmentioning

confidence: 73%

Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study

Dubois

Epelbaum

Nyasse

et al. 2018

The Lancet Neurology

181

207

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Section: Discussionmentioning

confidence: 73%

Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study

Dubois

Epelbaum

Nyasse

et al. 2018

The Lancet Neurology

181

207

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“…Several lines of evidence have pointed to the relation between Aβ and tau in the pathogenesis of AD; Aβ induces tau phosphorylation, accelerates NFT formation, and enhances tau pathology, or misfolded Aβ induces prion-like misfolded tau oligomers [13,14,30]. Tau aggregation is shown to precede β-amyloid deposits by about 30 years [31,32]. To date, none of Aβ-directed drugs for AD therapy have been successful and, therefore, a current target for AD therapy focuses on tau.…”

Section: Discussionmentioning

confidence: 99%

Combination of PKCε Activation and PTP1B Inhibition Effectively Suppresses Aβ-Induced GSK-3β Activation and Tau Phosphorylation

et al. 2015

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Glycogen synthase kinase-3β (GSK-3β) is a key element to phosphorylate tau and form neurofibrillary tangles (NFTs) found in tauopathies including Alzheimer's disease (AD). A current topic for AD therapy is focused upon how to prevent tau phosphorylation. In the present study, PKCε activated Akt and inactivated GSK-3β by directly interacting with each protein. Inhibition of protein tyrosine phosphatase 1B (PTP1B), alternatively, caused an enhancement in the tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1), allowing activation of Akt through a pathway along an IRS-1/phosphatidylinositol 3 kinase (PI3K)/3-phosphoinositide-dependent protein kinase-1 (PDK1)/Akt axis, to phosphorylate and inactivate GSK-3β. Combination of PKCε activation and PTP1B inhibition more sufficiently activated Akt and inactivated GSK-3β than each independent treatment, to suppress amyloid β (Aβ)-induced tau phosphorylation and ameliorate spatial learning and memory impairment in 5xFAD transgenic mice, an animal model of AD. This may represent an innovative strategy for AD therapy.

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“…According to the currently widely held model of AD pathogenesis, neurofibrillary tangle formation is secondary to amyloid plaque accumulation (Hardy, 2006), suggesting that taurelated atrophy might follow amyloid accumulation with a temporal delay and might also be regionally dissociated. An alternative account of recent findings would suggest that amyloid changes and tau pathology evolve as partly independent, but synergistic processes in AD pathogenesis (Duyckaerts, 2011), in which tau pathology in the transentorhinal and hippocampus region is an early but not the first event in AD pathology (Grinberg et al, 2009), leaving space for further dynamic processes of hippocampus atrophy in the course of manifest disease.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic basal forebrain atrophy predicts amyloid burden in Alzheimer's disease

Teipel

Heinsen

Amaro

et al. 2014

Neurobiology of Aging

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We compared accuracy of hippocampus and basal forebrain cholinergic system (BFCS) atrophy to predict cortical amyloid burden in 179 cognitively normal subjects (CN), 269 subjects with early stages of mild cognitive impairment (MCI), 136 subjects with late stages of MCI, and 86 subjects with Alzheimer’s disease (AD) dementia retrieved from the Alzheimer’s Disease Neuroimaging Initiative database. Hippocampus and BFCS volumes were determined from structural magnetic resonance imaging scans at 3 Tesla, and cortical amyloid load from AV45 (florbetapir) positron emission tomography scans. In receiver operating characteristics analyses, BFCS volume provided significantly more accurate classification into amyloid-negative and -positive categories than hippocampus volume. In contrast, hippocampus volume more accurately identified the diagnostic categories of AD, late and early MCI, and CN compared with whole and anterior BFCS volume, whereas posterior BFCS and hippocampus volumes yielded similar diagnostic accuracy. In logistic regression analysis, hippocampus and posterior BFCS volumes contributed significantly to discriminate MCI and AD from CN, but only BFCS volume predicted amyloid status. Our findings suggest that BFCS atrophy is more closely associated with cortical amyloid burden than hippocampus atrophy in predementia AD.

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Tau pathology in children and young adults: can you still be unconditionally baptist?

Cited by 63 publications

References 16 publications

Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study

Cognitive and neuroimaging features and brain β-amyloidosis in individuals at risk of Alzheimer's disease (INSIGHT-preAD): a longitudinal observational study

Combination of PKCε Activation and PTP1B Inhibition Effectively Suppresses Aβ-Induced GSK-3β Activation and Tau Phosphorylation

Cholinergic basal forebrain atrophy predicts amyloid burden in Alzheimer's disease

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