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Showing 1–18 of 18 results
Advanced filters: Author: Tara L. Spires-Jones Clear advanced filters

  • To mark the 20th anniversary of Nature Reviews Neuroscience, in this Viewpoint article we asked some of the researchers who have authored pieces published in the journal in recent years for their views on how the field, and their areas within it, have developed over the past two decades.

    • Danielle S. Bassett
    • Kathleen E. Cullen
    • Hiroki R. Ueda
    Reviews
    Nature Reviews Neuroscience
    Volume: 21, P: 524-534

  • Here, Spires-Jones and colleagues review our current understanding of the mechanisms underlying synaptic degeneration in Alzheimer disease and highlight key questions that still need to be answered. They also discuss novel therapeutic approaches that target the synapse.

    • Makis Tzioras
    • Robert I. McGeachan
    • Tara L. Spires-Jones
    Reviews
    Nature Reviews Neurology
    Volume: 19, P: 19-38

  • Alzheimer’s disease (AD) research is hampered by a lack of models that recapitulate all key disease features. Park et al. introduce a microfluidic device containing a 3D culture of human neurons, astrocytes, and microglia that develop AD-like pathology, revealing a potentially important inflammatory mechanism of neurodegeneration.

    • Christopher M. Henstridge
    • Tara L. Spires-Jones
    News & Views
    Nature Neuroscience
    Volume: 21, P: 899-900

  • Smoking remains a leading cause of preventable death and disease. Here, the authors explore the link between smoking and DNA methylation using arrays and next generation sequencing, and develop mCigarette, an epigenetic biomarker of smoking.

    • Aleksandra D. Chybowska
    • Elena Bernabeu
    • Riccardo E. Marioni
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-13

  • Senile plaques are thought to accumulate over the course of decades in brains of Alzheimer's disease patients. In vivo mutiphoton microscopy is used to follow the birth of such plaques in live Alzheimer's disease model mice. It is found that plaques form extraordinarily quickly, over 24 hours. Within 1–2 days, the microglia move in and noticeable neuritic changes ensue. These data argue that neuritic dysfunction follows, rather than precedes, amyloid deposition.

    • Melanie Meyer-Luehmann
    • Tara L. Spires-Jones
    • Bradley T. Hyman
    Research
    Nature
    Volume: 451, P: 720-724

  • Fibrillar deposits of tau protein (neurofibrillary tangles) are thought to cause neuronal death in patients with Alzheimer's disease, and tau-related frontotemporal dementia. Here, however, the opposite has been found: the activation of executioner caspase enzymes occurs first, preceding tangle formation by hours to days. Tangle-bearing neurons seem to be long-lived, indicating that tangles might be 'off pathway' to acute neuronal death.

    • Alix de Calignon
    • Leora M. Fox
    • Bradley T. Hyman
    Research
    Nature
    Volume: 464, P: 1201-1204

  • Mislocalisation of tau occurs in several neurodegenerative diseases and is thought to contribute to synaptic function. The authors show that presynaptically, tau binds to synaptic vesicles via the N-terminus which contributes to synaptic dysfunction.

    • Lujia Zhou
    • Joseph McInnes
    • Patrik Verstreken
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-13

  • The immediate-early gene Arc mediates synaptic plasticity and long-term memory formation. Whether Arc is dysregulated by amyloid-beta or in Alzheimer's disease is controversial. Here, a study used a reporter mouse line expressing destabilized fluorescent protein Venus under the control of the Arc promoter to show that Arc induction pattern, brain regional difference and precise location of active neurons with respect to senile plaque are major determinants of differential Arc response in a mouse model of Alzheimer's disease.

    • Nikita Rudinskiy
    • Jonathan M Hawkes
    • Bradley T Hyman
    Research
    Nature Neuroscience
    Volume: 15, P: 1422-1429

  • Understanding the complex interplay of cells that protect neurons early in Alzheimer disease but later contribute to neurodegeneration is important for developing effective therapeutics. In this Review, Henstridge and colleagues discuss the contributions of multiple cell types to disease pathogenesis.

    • Christopher M. Henstridge
    • Bradley T. Hyman
    • Tara L. Spires-Jones
    Reviews
    Nature Reviews Neuroscience
    Volume: 20, P: 94-108