From Science Advances, 27 February 2015. Click on the link to read the full text. Our website reflects some of the worldwide coverage of this item
Distinct plasma immune signatures in ME/CFS are present early in the course of illness
Mady Hornig(1,2,*), José G. Montoya(3), Nancy G. Klimas(4), Susan Levine(5), Donna Felsenstein(6), Lucinda Bateman(7), Daniel L. Peterson(8), C. Gunnar Gottschalk(8), Andrew F. Schultz(1), Xiaoyu Che(1), Meredith L. Eddy(1), Anthony L. Komaroff(9) and W. Ian Lipkin(1,2,10).
1) Center for Infection and Immunity, Columbia University Mailman School of Public Health, New York, NY 10032, USA.
2) Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY 10032, USA.
3) Stanford University, Palo Alto, CA 94305, USA.
4)Institute for Neuro-Immune Medicine, College of Osteopathic Medicine, Nova Southeastern University, Fort Lauderdale, FL 33314, USA, and Miami VA Medical Center, Miami, FL 33125, USA.
5) Levine Clinic, New York, NY 10021, USA.
6) Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
7) Fatigue Consultation Clinic, Salt Lake City, UT 84102, USA.
8) Sierra Internal Medicine at Incline Village, Incline Village, NV 89451, USA.
9) Harvard Medical School, Brigham and Women’s Hospital, Boston, MA 02115, USA.
10)Departments of Neurology and Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
*Corresponding author. E-mail: email@example.com
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an unexplained incapacitating illness that may affect up to 4 million people in the United States alone. There are no validated laboratory tests for diagnosis or management despite global efforts to find biomarkers of disease.
We considered the possibility that inability to identify such biomarkers reflected variations in diagnostic criteria and laboratory methods as well as the timing of sample collection during the course of the illness. Accordingly, we leveraged two large, multicenter cohort studies of ME/CFS to assess the relationship of immune signatures with diagnosis, illness duration, and other clinical variables. Controls were frequency-matched on key variables known to affect immune status, including season of sampling and geographic site, in addition to age and sex.
We report here distinct alterations in plasma immune signatures early in the course of ME/CFS (n = 52) relative to healthy controls (n = 348) that are not present in subjects with longer duration of illness (n = 246). Analyses based on disease duration revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines as well as dissociation of intercytokine regulatory networks.
We found a stronger correlation of cytokine alterations with illness duration than with measures of illness severity, suggesting that the immunopathology of ME/CFS is not static. These findings have critical implications for discovery of interventional strategies and early diagnosis of ME/CFS.
From the Journal of Clinical Rheumatology, 2 March 2015.
Cross-sectional Neurocognitive Data Do Not Support a Transition From Fibrofog to Alzheimer Disease in Fibromyalgia Patients.
Leavitt F, Katz RS.
Department of Behavioral Sciences and †Section of Rheumatology, Department of Internal Medicine, Rush Medical College, Chicago, IL.
Cognitive dysfunction is a signature feature of fibromyalgia. Many who develop cognitive problems in their middle years are concerned that it is prodromal to Alzheimer’s disease.
To determine if deficits in episodic memory and progressive cognitive decline, hallmarks of Alzheimer’s disease, are prominent in the cognitive makeup of fibromyalgia patients.
In a cross-sectional study, performance on 15 neurocognitive (NC) measures was evaluated in 2 cohorts of fibromyalgia subjects. The first cohort contained 94 subjects with a short duration of cognitive problems (≤12 months). The second cohort contained 55 subjects with a long duration of cognitive problems (≥84 months).
The 2 groups were similar in education (14.9 ± 2.3 vs 14.9 ± 2.4), vocabulary scale score (11.2 ± 2.3 vs 11.6 ± 2.7), and depression (17.9 ± 9.8 vs 17.7 ± 9.4). The mean durations of cognitive problems in the short- and long-term group were 7.3 ± 3.9 months and 13.3 ± 7.1 years, respectively. There was no evidence of decline on 14 of 15 measures in the fibromyalgia group with an additional 12.6 years of cognitive dysfunction. Normality of function was in evidence on 4 measures of episodic memory in both cohorts.
Fibromyalgia patients’ fear of developing Alzheimer’s disease was not borne out by the data. The cognitive pattern of fibromyalgia appears distinct from that of Alzheimer’s disease.
Fibrofog is not associated with either episodic memory loss on standard tests of episodic memory or progressive cognitive decline. Patients with fibrofog remember personally experienced events termed episodic memory at a normal rate in quiet, distraction-free conditions. Patients with Alzheimer’s disease do not. They forget the essential elements of short stories just read to them in environments free of distractions.
In Alzheimer’s disease, the brain mechanisms responsible for encoding personally experienced events into memory are irreversibly impaired. In fibrofog, the encoding mechanisms are intact.
At the heart of memory loss in fibromyalgia is the inability to appropriately filter out relevant distractions. Encoding mechanisms that otherwise operate normally in forming episodic memories for everyday events in fibromyalgia appear to malfunction when 2 streams of information operate concurrently (relevant information and a source of distraction overlap).
The findings should allay the worries of many with fibromyalgia who fear that fibrofog is the start of a dementing process.
From Ross Fiziol Zh Im I M Sechenova, May 2014.
Impairments of rats’ behavioral reactions, concentration of corticosterone and expression of cytokine’s gene under experimental postviral fatigue.
[Article in Russian]
Filatenkova TA, Dmitrienko EV, Fomicheva EE, Shanin SN, Rybakina EG.
The aim of the main research was investigated of interaction of neural, endocrine and immune systems under experimental post viral fatigue, behavioral reactions, level of corticosterone, changes of IL-3 and IL-10 gene expression in rats’ hypothalamus and INF-α in hypothalamus and spleen were analyzed.
It has been shown the decrease of physical activity, increasing of corticosterone’s level and gene expression of cytokines after injection of Poly I:C as a model of postviral fatigue. After remedication of Poly I:C increasing of physical activity was shown.