Journal: Neurodegenerative Diseases

Abbreviation

Neurodegener. Dis.

Publisher

Karger

Journal Volumes

ISSN

1660-2854
1660-2862

Description

Filters

Reset filters

Search Results

Publications 1 - 10 of 13
  • Trials of Antidliabetic Drugs in Amyotrophic Lateral Sclieros
    Item type: Journal Article
    Jawaid, A.; Paganoni, S.; Hauser, C.; et al. (2014)
    Neurodegenerative Diseases
  • Effects of Arm Training with the Robotic Device ARMin I in Chronic Stroke: Three Single Cases
    Item type: Journal Article
    Nef, Tobias; Quinter, Gabriela; Müller, Roland; et al. (2010)
    Neurodegenerative Diseases
    Background:Several clinical studies on chronic stroke conducted with end-effector-based robots showed improvement of the motor function in the affected arm. Compared to end-effector-based robots, exoskeleton robots provide improved guidance of the human limb and are better suited to train task-oriented movements with a large range of motions. Objective: To test whether intensive arm training with the arm exoskeleton ARMin I is feasible with chronic-stroke patients and whether it improves motor function in the paretic arm. Methods: Three single cases with chronic hemiparesis resulting from unilateral stroke (at least 14 months after stroke). A-B design with 2 weeks of multiple baseline measurements (A), 8 weeks of training (B) with repetitive measurements and a follow-up measurement 8 weeks after training. The training included shoulder and elbow movements with the robotic rehabilitation device ARMin I. Two subjects had three 1-hour sessions per week and 1 subject received five 1-hour sessions per week. The main outcome measurement was the upper-limb part of the Fugl-Meyer Assessment (FMA). Results:The ARMin training was well tolerated by the patients, and the FMA showed moderate, but significant improvements for all 3 subjects (p < 0.05). Most improvements were maintained 8 weeks after discharge. Conclusions: This study indicates that intensive training with an arm exoskeleton is feasible with chronic-stroke patients. Moderate improvements were found in all 3 subjects, thus further clinical investigations are justified. © 2009 S. Karger AG, Basel
  • Repair of the injured spinal cord
    Item type: Journal Article
    Buchli, Anita D.; Rouiller, Eric; Mueller, Roland; et al. (2007)
    Neurodegenerative Diseases
  • Adenosine-based cell therapy approaches for pharmacoresistant epilepsies
    Item type: Journal Article
    Boison, Detlev (2007)
    Neurodegenerative Diseases
  • Physician and Surrogate Agreement with Assisted Dying and Continuous Deep Sedation in Advanced Dementia in Switzerland
    Item type: Journal Article
    Loizeau, Andrea; Cohen, Simon M.; Mitchell, Susan L.; et al. (2019)
    Neurodegenerative Diseases
  • An Integrated View on Vascular Dysfunction in Alzheimer’s Disease
    Item type: Review Article
    Klohs, Jan (2020)
    Neurodegenerative Diseases
    Background: Cerebrovascular disease is a common comorbidity in patients with Alzheimer’s disease (AD). It is believed to contribute additively to the cognitive impairment and to lower the threshold for the development of dementia. However, accumulating evidence suggests that dysfunction of the cerebral vasculature and AD neuropathology interact in multiple ways. Vascular processes even proceed AD neuropathology, implicating a causal role in the etiology of AD. Thus, the review aims to provide an integrated view on vascular dysfunction in AD. Summary: In AD, the cerebral vasculature undergoes pronounced cellular, morphological and structural changes, which alters regulation of blood flow, vascular fluid dynamics and vessel integrity. Stiffening of central blood vessels lead to transmission of excessive pulsatile energy to the brain microvasculature, causing end-organ damage. Moreover, a dysregulated hemostasis and chronic vascular inflammation further impede vascular function, where its mediators interact synergistically. Changes of the cerebral vasculature are triggered and driven by systemic vascular abnormalities that are part of aging, and which can be accelerated and aggravated by cardiovascular diseases. Key Messages: In AD, the cerebral vasculature is the locus where multiple pathogenic processes converge and contribute to cognitive impairment. Understanding the molecular mechanism and pathophysiology of vascular dysfunction in AD and use of vascular blood-based and imaging biomarker in clinical studies may hold promise for future prevention and therapy of the disease.
  • Amyloid-β Aggregation
    Item type: Journal Article
    Finder, Verena H.; Glockshuber, Rudi (2007)
    Neurodegenerative Diseases
  • New Technologies and Concepts for Rehabilitation in the Acute Phase of Stroke
    Item type: Journal Article
    Siekierka, E.M.; Eng, K.; Bassetti, C.; et al. (2007)
    Neurodegenerative Diseases
  • Direct Evidence for Self-Propagation Different Amyloid-β Fibril Conformations
    Item type: Journal Article
    Spirig, Thomas; Ovchinnikova, Oxana; Vagt, Toni; et al. (2014)
    Neurodegenerative Diseases
    Background: Amyloid fibrils formed by amyloid-β (Aβ) peptides are associated with Alzheimer's disease and can occur in a range of distinct morphologies that are not uniquely determined by the Aβ sequence. Whether distinct conformations of Aβ fibrils can be stably propagated over multiple cycles of seeding and fibril growth has not been established experimentally. Objective: The ability of the 40-residue peptide Aβ1-40 to assemble into fibrils with the conformation of the mutant Aβ1-40 peptide containing the ‘Osaka' mutation E22Δ was investigated. Methods: Fibril formation of highly pure, recombinant Aβ1-40 in the presence of distinct, preformed seeds in vitro was recorded with thioflavin T fluorescence, and distinct fibrillar structures were identified and distinguished by fluorescence spectroscopy and electron microscopy. Results: We propagated the specific quaternary structure of Aβ1-40 E22Δ fibrils with wild-type Aβ1-40 over up to seven cycles of seeding and fibril elongation. As a result of a 10⁷-fold dilution of the initially present Aβ1-40 E22Δ seeds, the vast majority of fibrils formed after the seventh propagation cycle with Aβ1-40 did not contain a single molecule of Aβ1-40 E22Δ, but still retained the conformation of the initial Aβ1-40 E22Δ seeds. Increased critical concentrations of Aβ1-40 fibrils formed in the presence of Aβ1-40 E22Δ nuclei suggest that these fibrils are less stable than homologously seeded Aβ1-40 fibrils, consistent with a kinetically controlled mechanism of fibril formation. Conclusion: The propagation of a distinct Aβ fibril conformation over multiple cycles of seeded fibril growth demonstrates the basic ability of the Aβ peptide to form amyloid strains that in turn may cause phenotypes in Alzheimer's disease.
  • Cortical Plasticity
    Item type: Journal Article
    Kiper, Daniel C.; Martin, Kevan A.C.; Scherberger, Hans J. (2007)
    Neurodegenerative Diseases
Publications 1 - 10 of 13