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Reduced N-acetylaspartate in Hippocampus of Fibromyalgia Patients

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www.ProHealth.com • July 17, 2013


Editor's comment: N-acetylaspartate (NAA), the acetylated form of the amino acid aspartate, is the second most abundant metabolite in the human central nervous system, following only the amino acid glutamate.  NAA emits the strongest signal in magnetic resonance spectrograms of the brain.  NAA levels are known to be altered in a large number of central nervous system disorders and are almost always reduced in neurological disorders involving neuronal loss or dysfunction. 

Reduced N-acetylaspartate in the hippocampus in patients with fibromyalgia: A meta-analysis.

By Yuta Aoki, Ryota Inokuchi and Hiroshi Suwa

Abstract:

Fibromyalgia (FM) is a stress-associated syndrome with chronic, widespread pain. Patients with FM also present disturbances of cognition and memory.

As the hippocampus is vulnerable to stress exposure and involved in cognition, memory and pain perception, we hypothesize that the abnormal function of the hippocampus is implicated in the pathophysiology of FM.

N-acetylaspartate (NAA), a metabolite that can be measured using proton magnetic resonance spectroscopy (1H MRS), is recognized as a marker of neuronal structure and function. We performed a systematic review and meta-analysis of 1H MRS studies investigating NAA levels in patients with FM.  A comprehensive literature search through MEDLINE, Embase and Web of Science yielded nine studies; among these nine, four studies met our criteria for inclusion.

A random effect model with 51 patients with FM and 38 controls revealed a significant NAA reduction in the hippocampus. The current meta-analysis suggested a neuronal abnormality in the hippocampus in patients with FM.

Source: Psychiatry Research, July 5, 2013. By Yuta Aoki, Ryota Inokuchi and Hiroshi Suwa. Department of Psychiatry, Tokyo Metropolitan Health and Medical Treatment Corporation, Ebara Hospital, Ota, Tokyo 145-0065, Japan; Department of Emergency Medicine and Critical Care Medicine, The University of Tokyo Hospital, Bunkyou, Tokyo 113-8655, Japan.





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