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    1. Neuroscience

    Sleep is bi-directionally modified by amyloid beta oligomers

    Güliz Gürel Özcan et al.
    Amyloid beta, the major component of plaques in Alzheimer's disease, acutely and reversibly signals to modulate sleep as a function of oligomeric length, independently of neuronal loss.
    1. Neuroscience

    Loss of presenilin function is associated with a selective gain of APP function

    Carole Deyts et al.
    Amyloid precursor protein expression and accumulation of its intracellular fragment are required for exuberant neurite outgrowth associated with pathological presenilin 1 loss-of-function mutations before the emergence of amyloid burden in mice.
    1. Neuroscience

    TrpV1 receptor activation rescues neuronal function and network gamma oscillations from Aβ-induced impairment in mouse hippocampus in vitro

    Hugo Balleza-Tapia et al.
    TrpV1 receptor activation rescues cognition-relevant network dynamics in mouse hippocampus in an acute Alzheimer disease model providing a novel therapeutic target.
    1. Neuroscience

    Amyloid and tau accumulate across distinct spatial networks and are differentially associated with brain connectivity

    Joana B Pereira et al.
    The amyloid patterns overlap with the default-mode network, whereas the tau patterns overlap with distinct functional networks and are associated with a loss of anatomical connectivity and multiple cognitive functions.
    1. Computational and Systems Biology
    2. Neuroscience

    Differences in topological progression profile among neurodegenerative diseases from imaging data

    Sara Garbarino et al.
    Computational-driven, imaging-based topological profiles of neurodegeneration differ substantially in different neurodegenerative conditions, suggesting distinct modes of dependence of the pathological spread on the underlying connectivity.
    1. Neuroscience

    Oscillatory hyperactivity and hyperconnectivity in young APOE-ɛ4 carriers and hypoconnectivity in Alzheimer’s disease

    Loes Koelewijn et al.
    Electrophysiology pinpoints brain function abnormalities in young people genetically at risk of developing Alzheimer's disease much later in life, supporting theories of initial hyperconnectivity driving eventual profound disconnection.
    1. Biochemistry and Chemical Biology
    2. Neuroscience

    Somatostatin binds to the human amyloid β peptide and favors the formation of distinct oligomers

    Hansen Wang et al.
    The cyclic neuropeptide somatostatin binds to human Aβ1-42 through an interface that critically relies on a specific tryptophan, thereby blocking the propensity of Aβ to aggregate, a critical step in the pathobiology of Alzheimer's disease.
    1. Neuroscience

    Neuropathological and transcriptomic characteristics of the aged brain

    Jeremy A Miller et al.
    High variability in neuropathology burden and interactions between dementia diagnosis and RNA quality present underappreciated complications when studying dementia in an aged population.
    1. Developmental Biology
    2. Neuroscience

    APP interacts with LRP4 and agrin to coordinate the development of the neuromuscular junction in mice

    Hong Y Choi et al.
    Proteins implicated in Alzheimer’s disease, including amyloid precursor protein and ApoE receptors, interact with each other and with a signalling molecule called agrin to influence the development of the neuromuscular junction.
    1. Structural Biology and Molecular Biophysics
    2. Neuroscience

    Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms

    Daniel L Kober et al.
    Structural, biophysical, and functional analyses reveal that mutations in TREM2 trigger either misfolding or reduced binding to cell-surface glycosaminoglycans, which segregate with neurodegenerative disease link and highlight a functional surface linked to the pathogenesis of Alzheimer's disease.