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Ann Neurol. 2011 Mar;69(3):445-54. doi: 10.1002/ana.22337.

Demyelination causes synaptic alterations in hippocampi from multiple sclerosis patients.

Author information

1
Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, OH 44195, USA.

Abstract

OBJECTIVE:

Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the human central nervous system. Although the clinical impact of gray matter pathology in MS brains is unknown, 30 to 40% of MS patients demonstrate memory impairment. The molecular basis of this memory dysfunction has not yet been investigated in MS patients.

METHODS:

To investigate possible mechanisms of memory impairment in MS patients, we compared morphological and molecular changes in myelinated and demyelinated hippocampi from postmortem MS brains.

RESULTS:

Demyelinated hippocampi had minimal neuronal loss but significant decreases in synaptic density. Neuronal proteins essential for axonal transport, synaptic plasticity, glutamate neurotransmission, glutamate homeostasis, and memory/learning were significantly decreased in demyelinated hippocampi, but not in demyelinated motor cortices from MS brains.

INTERPRETATION:

Collectively, these data support hippocampal demyelination as a cause of synaptic alterations in MS patients and establish that the neuronal genes regulated by myelination reflect specific functions of neuronal subpopulations.

PMID:
21446020
PMCID:
PMC3073544
DOI:
10.1002/ana.22337
[Indexed for MEDLINE]
Free PMC Article
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