Journal: Annals of Neurology

Abbreviation

Ann Neurol

Publisher

Wiley

Journal Volumes

ISSN

0364-5134
1531-8249

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Publications 1 - 10 of 12
  • Neurotrophic cross-talk between the nervous and immune systems
    Item type: Journal Article
    Kerschensteiner, Martin; Stadelmann, Christine; Dechant, Georg; et al. (2003)
    Annals of Neurology
  • Recovery and brain reorganization after stroke in adult and aged rats
    Item type: Journal Article
    Markus, Tiffanie M.; Tsai, Shih-Yen; Bollnow, Melanie R.; et al. (2005)
    Annals of Neurology
  • Early Aβ reduction prevents progression of cerebral amyloid angiopathy
    Item type: Journal Article
    Schelle, Juliane; Wegenast-Braun, Bettina M.; Fritschi, Sarah K.; et al. (2019)
    Annals of Neurology
    Objective Clinical trials targeting β‐amyloid peptides (Aβ) for Alzheimer disease (AD) failed for arguable reasons that include selecting the wrong stages of AD pathophysiology or Aβ being the wrong target. Targeting Aβ to prevent cerebral amyloid angiopathy (CAA) has not been rigorously followed, although the causal role of Aβ for CAA and related hemorrhages is undisputed. CAA occurs with normal aging and to various degrees in AD, where its impact and treatment is confounded by the presence of parenchymal Aβ deposition. Methods APPDutch mice develop CAA in the absence of parenchymal amyloid, mimicking hereditary cerebral hemorrhage with amyloidosis Dutch type (HCHWA‐D). Mice were treated with a β‐site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor. We used 3‐dimensional ultramicroscopy and immunoassays for visualizing CAA and assessing Aβ in cerebrospinal fluid (CSF) and brain. Results CAA onset in mice was at 22 to 24 months, first in frontal leptomeningeal and superficial cortical vessels followed by vessels penetrating the cortical layers. CSF Aβ increased with aging followed by a decrease of both Aβ40 and Aβ42 upon CAA onset, supporting the idea that combined reduction of CSF Aβ40 and Aβ42 is a specific biomarker for vascular amyloid. BACE1 inhibitor treatment starting at CAA onset and continuing for 4 months revealed a 90% Aβ reduction in CSF and largely prevented CAA progression and associated pathologies. Interpretation This is the first study showing that Aβ reduction at early disease time points largely prevents CAA in the absence of parenchymal amyloid. Our observation provides a preclinical basis for Aβ‐reducing treatments in patients at risk of CAA and in presymptomatic HCHWA‐D.
  • Neural basis of induced phantom limb pain relief
    Item type: Journal Article
    Kikkert, Sanne; Mezue, Melvin; O'Shea, Jacinta; et al. (2019)
    Annals of Neurology
    Objective Phantom limb pain (PLP) is notoriously difficult to treat, partly due to an incomplete understanding of PLP‐related disease mechanisms. Noninvasive brain stimulation (NIBS) is used to modulate plasticity in various neuropathological diseases, including chronic pain. Although NIBS can alleviate neuropathic pain (including PLP), both disease and treatment mechanisms remain tenuous. Insight into the mechanisms underlying both PLP and NIBS‐induced PLP relief is needed for future implementation of such treatment and generalization to related conditions. Methods We used a within‐participants, double‐blind, and sham‐controlled design to alleviate PLP via task‐concurrent NIBS over the primary sensorimotor missing hand cortex (S1/M1). To specifically influence missing hand signal processing, amputees performed phantom hand movements during anodal transcranial direct current stimulation. Brain activity was monitored using neuroimaging during and after NIBS. PLP ratings were obtained throughout the week after stimulation. Results A single session of intervention NIBS significantly relieved PLP, with effects lasting at least 1 week. PLP relief associated with reduced activity in the S1/M1 missing hand cortex after stimulation. Critically, PLP relief and reduced S1/M1 activity correlated with preceding activity changes during stimulation in the mid‐ and posterior insula and secondary somatosensory cortex (S2). Interpretation The observed correlation between PLP relief and decreased S1/M1 activity confirms our previous findings linking PLP with increased S1/M1 activity. Our results further highlight the driving role of the mid‐ and posterior insula, as well as S2, in modulating PLP. Lastly, our novel PLP intervention using task‐concurrent NIBS opens new avenues for developing treatment for PLP and related pain conditions. ANN NEUROL 2019;85:59–73.
  • Abnormal junctions and permeability of myelin in PMP22-deficient nerves
    Item type: Journal Article
    Guo, Jiasong; Wang, Leiming; Zhang, Yang; et al. (2014)
    Annals of Neurology
  • Abnormal activity in reward brain circuits in human narcolepsy with cataplexy
    Item type: Journal Article
    Ponz, A.; Khatami, R.; Poryazova, R.; et al. (2010)
    Annals of Neurology
  • Six-Month Assessment of a Hand Prosthesis with Intraneural Tactile Feedback
    Item type: Journal Article
    Petrini, Francesco M.; Valle, Giacomo; Strauss, Ivo; et al. (2019)
    Annals of Neurology
  • Reduced amygdala activity during aversive conditioning in human narcolepsy
    Item type: Journal Article
    Ponz, A.; Khatami, R.; Poryazova, R.; et al. (2010)
    Annals of Neurology
  • Nogo-A antibody improves regeneration and locomotion of spinal cord-injured rats
    Item type: Journal Article
    Liebscher, Thomas; Schnell, Lisa; Schnell, Dina; et al. (2005)
    Annals of Neurology
  • Nogo-A antibodies and training reduce muscle spasms in spinal cord-injured rats
    Item type: Journal Article
    Gonzenbach, Roman R.; Gasser, Pascal; Zörner, Björn; et al. (2010)
    Annals of Neurology
Publications 1 - 10 of 12