| Cognitive and cortical plasticity deficits correlate with altered amyloid-β CSF levels in multiple sclerosis. | |
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MedLine Citation:
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PMID: 20944553 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cognitive dysfunction is of frequent observation in multiple sclerosis (MS). It is associated with gray matter pathology, brain atrophy, and altered connectivity, and recent evidence showed that acute inflammation can exacerbate mental deficits independently of the primary functional system involved. In this study, we measured cerebrospinal fluid (CSF) levels of amyloid-β(1-42) and τ protein in MS and in clinically isolated syndrome patients, as both proteins have been associated with cognitive decline in Alzheimer's disease (AD). In AD, amyloid-β(1-42) accumulates in the brain as insoluble extracellular plaques, possibly explaining why soluble amyloid-β(1-42) is reduced in the CSF of these patients. In our sample of MS patients, amyloid-β(1-42) levels were significantly lower in patients cognitively impaired (CI) and were inversely correlated with the number of Gadolinium-enhancing (Gd+) lesions at the magnetic resonance imaging (MRI). Positive correlations between amyloid-β(1-42) levels and measures of attention and concentration were also found. Furthermore, abnormal neuroplasticity of the cerebral cortex, explored with θ burst stimulation (TBS), was observed in CI patients, and a positive correlation was found between amyloid-β(1-42) CSF contents and the magnitude of long-term potentiation-like effects induced by TBS. No correlation was conversely found between τ protein concentrations and MRI findings, cognitive parameters, and TBS effects in these patients. Together, our results indicate that in MS, central inflammation is able to alter amyloid-β metabolism by reducing its concentration in the CSF and leading to impairment of synaptic plasticity and cognitive function. |
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Authors:
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Francesco Mori; Silvia Rossi; Giulia Sancesario; Claudia Codecà; Giorgia Mataluni; Fabrizia Monteleone; Fabio Buttari; Hajime Kusayanagi; Maura Castelli; Caterina Motta; Valeria Studer; Giorgio Bernardi; Giacomo Koch; Sergio Bernardini; Diego Centonze |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-13 |
Journal Detail:
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Title: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology Volume: 36 ISSN: 1740-634X ISO Abbreviation: Neuropsychopharmacology Publication Date: 2011 Feb |
Date Detail:
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Created Date: 2011-01-13 Completed Date: 2011-05-09 Revised Date: 2012-02-01 |
Medline Journal Info:
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Nlm Unique ID: 8904907 Medline TA: Neuropsychopharmacology Country: United States |
Other Details:
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Languages: eng Pagination: 559-68 Citation Subset: IM |
Affiliation:
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Dipartimento di Neuroscienze, Clinica Neurologica, Università Tor Vergata, Rome, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Amyloid beta-Peptides / cerebrospinal fluid*, pharmacology Cerebral Cortex / pathology, physiopathology* Cognition Disorders / etiology* Evoked Potentials, Motor / physiology Female Functional Laterality Gadolinium / diagnostic use Humans Long-Term Potentiation / drug effects Magnetic Resonance Imaging / methods Male Middle Aged Multiple Sclerosis* / cerebrospinal fluid, complications, pathology Muscle, Skeletal / innervation Neuronal Plasticity / physiology* Neurons / drug effects, physiology Neuropsychological Tests Peptide Fragments / cerebrospinal fluid*, pharmacology Statistics as Topic Time Factors Transcranial Magnetic Stimulation Young Adult tau Proteins / cerebrospinal fluid |
| Chemical | |
Reg. No./Substance:
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0/Amyloid beta-Peptides; 0/Peptide Fragments; 0/amyloid beta-protein (1-42); 0/tau Proteins; 7440-54-2/Gadolinium |
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