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Amritpal Mudher
Researcher at University of Southampton
Publications - 43
Citations - 2078
Amritpal Mudher is an academic researcher from University of Southampton. The author has contributed to research in topics: Tau protein & Tauopathy. The author has an hindex of 20, co-authored 40 publications receiving 1789 citations. Previous affiliations of Amritpal Mudher include King's College London & University of Oxford.
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Journal ArticleDOI
Alzheimer's disease – do tauists and baptists finally shake hands?
Amritpal Mudher,Simon Lovestone +1 more
TL;DR: The finding of tau mutations in other dementias has added weight to the hypothesis as it suggests that tau-pathology is a downstream but essential part of the dementing process, however, some observations remain difficult to reconcile with the hypothesis.
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GSK-3beta inhibition reverses axonal transport defects and behavioural phenotypes in Drosophila.
Amritpal Mudher,David Shepherd,Tracey A. Newman,P Mildren,J P Jukes,A Squire,A Mears,S Berg,Daniel Mackay,Ayodeji A. Asuni,R Bhat,Simon Lovestone +11 more
TL;DR: The data show that tau abnormalities significantly disrupt neuronal function, in a phosphorylation-dependent manner, before the classical pathological hallmarks are evident and also suggest that the inhibition of GSK-3β might have potential therapeutic benefits in tauopathies.
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Alzheimer's Disease and Type 2 Diabetes: A Critical Assessment of the Shared Pathological Traits.
TL;DR: In this review, it is discussed how Insulin resistance in T2DM directly exacerbates Aβ and tau pathologies and elucidated the pathophysiological traits of synaptic dysfunction, inflammation, and autophagic impairments that are common to both diseases and indirectly impact Aβand tau functions in the neurons.
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Soluble hyper-phosphorylated tau causes microtubule breakdown and functionally compromises normal tau in vivo.
TL;DR: All these phospho-tau-mediated phenotypes occur in the absence of tau filament/neurofibrillary tangle formation or neuronal death, and may constitute the mechanism by which hyper-phosphorylated tau disrupts neuronal function and contributes to cognitive impairment prior to neuronal death in the early stages of t Tauopathies.
Journal ArticleDOI
Dishevelled regulates the metabolism of amyloid precursor protein via protein kinase C/mitogen-activated protein kinase and c-Jun terminal kinase.
Amritpal Mudher,Susan Chapman,J Richardson,Abdur-Rasheed Asuni,G M Gibb,Claire L. Pollard,Richard Killick,T Iqbal,L Raymond,Ian M. Varndell,Paul W. Sheppard,Andrew Makoff,E Gower,P E Soden,Patrick A. Lewis,Matthew C. Murphy,Todd E. Golde,H T Rupniak,Brian H. Anderton,Simon Lovestone +19 more
TL;DR: It is shown that human dvl-1 and wnt-1 also reduce the phosphorylation of tau by GSK-3β, suggesting that both APP metabolism and tauosphorylation are potentially linked through wnt signaling.