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Alzheimers Dement. 2015 Jan;11(1):40-50.e1-2. doi: 10.1016/j.jalz.2013.12.024. Epub 2014 Feb 12.

Resolution of inflammation is altered in Alzheimer's disease.

Author information

  • 1Department of Neurobiology, Care Sciences and Society, Section of Neurodegeneration, Karolinska Institutet, Stockholm, Sweden.
  • 2Department of Neurobiology, Care Sciences and Society, Section of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden.
  • 3Department of Laboratory Medicine, Section of Pathology, Karolinska Institutet, Stockholm, Sweden.
  • 4Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
  • 5Department of Neurosciences and the Center on Aging, Medical University of South Carolina, Charleston, SC, USA.
  • 6Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
  • 7Department of Neurobiology, Care Sciences and Society, Section of Neurodegeneration, Karolinska Institutet, Stockholm, Sweden. Electronic address: marianne.schultzberg@ki.se.

Abstract

BACKGROUND:

Resolution is the final stage of the inflammatory response, when restoration of tissue occurs. Failure may lead to chronic inflammation, which is known as part of the pathology in the brain of individuals with Alzheimer's disease (AD).

METHODS:

Specialized pro-resolving mediators (SPMs), receptors, biosynthetic enzyme, and downstream effectors involved in resolution were analyzed in postmortem hippocampal tissue from AD patients and non-AD subjects. SPMs were analyzed in cerebrospinal fluid (CSF).

RESULTS:

SPMs and SPM receptors were detected in the human brain. Levels of the SPM lipoxin A4 (LXA4) were reduced in AD, both in the CSF and hippocampus. An enzyme involved in LXA4 synthesis and two SPM receptors were elevated in AD brains. LXA4 and RvD1 levels in CSF correlated with Mini-Mental State Examination (MMSE) scores.

CONCLUSIONS:

A resolution pathway exists in the brain and the alterations described herein strongly suggest a dysfunction of this pathway in AD. MMSE correlations suggest a connection with cognitive function in AD.

Copyright © 2015 The Alzheimer's Association. All rights reserved.

KEYWORDS:

15-Lipoxygenase-2; ALX/FPR2; ChemR23; ELISA; FPRL1; Human; Immunohistochemistry; Lipoxin A(4); Mild cognitive impairment; Resolvin D1; Specialized pro-resolving mediators; Tau

PMID:
24530025
[PubMed - indexed for MEDLINE]
PMCID:
PMC4275415
Free PMC Article
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