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Showing 1–7 of 7 results
Advanced filters: Author: Marc Aurel Busche Clear advanced filters
  • Microscopic imaging of neurons in mouse models of Alzheimer’s disease shows that plaques increase activity while neurofibrillary tangles suppress activity. The combination of plaques and tangles, as in humans with Alzheimer’s disease, suppresses activity.

    • Marc Aurel Busche
    • Susanne Wegmann
    • Bradley T. Hyman
    Research
    Nature Neuroscience
    Volume: 22, P: 57-64
  • Immunotherapy with antibodies targeting the amyloid-β peptide has yet to show any cognitive benefit in Alzheimer's disease patients in clinical trials. In vivo two-photon imaging in mouse models of Alzheimer's disease now reveals that these antibodies do not alleviate neuronal dysfunction and can even worsen it.

    • Marc Aurel Busche
    • Christine Grienberger
    • Arthur Konnerth
    Research
    Nature Neuroscience
    Volume: 18, P: 1725-1727
  • Busche and Hyman review emerging evidence for an interaction between Aβ and tau during Alzheimer’s disease (AD) progression that challenges the classical linear trajectory model and offers a new perspective on AD pathophysiology and therapy.

    • Marc Aurel Busche
    • Bradley T. Hyman
    Reviews
    Nature Neuroscience
    Volume: 23, P: 1183-1193
  • Sleeping mammalian brains show high coherence of slow-wave activity. In mouse models of Alzheimer's disease, which have abnormal levels of amyloid-β, amyloid plaques and associated memory deficits, these waves are massively impaired. This impairment is related to the previously demonstrated neuronal hyperactivity. Pharmacological manipulations that reduce hyperactivity result in the reinstatement of slow-wave coherence and in memory improvement.

    • Marc Aurel Busche
    • Maja Kekuš
    • Arthur Konnerth
    Research
    Nature Neuroscience
    Volume: 18, P: 1623-1630
  • β-amyloid (Aβ)-dependent neuronal hyperactivity is an early marker of Alzheimer’s Disease (AD). Here, the authors report that scavenging Aβ monomers by an Aβ-binding anticalin protein blocks the formation of Aβ oligomers and prevents hyperactivity in AD mice.

    • Benedikt Zott
    • Lea Nästle
    • Arthur Konnerth
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-13
  • C9orf72 ALS/FTD polyGR and polyPR knock-in mice show cortical hyperexcitability and motor neuron loss accompanied by an increase in extracellular matrix proteins in the spinal cord that is conserved in patient iPS cell-derived neurons and is neuroprotective.

    • Carmelo Milioto
    • Mireia Carcolé
    • Adrian M. Isaacs
    ResearchOpen Access
    Nature Neuroscience
    Volume: 27, P: 643-655
  • A new pathway for the processing of β-amyloid precursor protein (APP) is described in which η-secretase activity, in part mediated by the MT5-MMP metalloproteinase, cleaves APP, and further processing by ADAM10 and BACE1 generates proteolytic fragments capable of inhibiting long-term potentiation in the hippocampus.

    • Michael Willem
    • Sabina Tahirovic
    • Christian Haass
    Research
    Nature
    Volume: 526, P: 443-447