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Unger: telomeerlengte aanzienlijk korter in CVS

 

 

 

 


 

 

https://commons.wikimedia.org/w/index.php?curid=75190

 

 

Volgens een recent verschenen studie van Unger (CDC) zijn de lengte van de telomeren

van patiŰnten met "CVS" en chronische vermoeidheid korter dan die van gezonde proefpersonen.

 

Toelichting:

 

Telomeren zijn repeterende stukjes DNA die belangrijke genen beschermen tegen het

korter worden van de chromosomen. Tijdens de celdeling wordt het DNA via replicatie verdubbeld.

Het enzym DNA-polymerase kan echter het eind van het chromosoom niet repliceren, omdat

het voortijdig van het DNA afvalt. Hierdoor worden bij elke celdeling de chromosomen iets korter.

 

Als het DNA te veel beschadigd is en niet meer hersteld kan worden, stopt de cel met delen of gaat dood. Als het telomeer 4 kilobasen kort is geworden, ziet het DNA-herstelmechanisme het eind

van het chromosoom als een gebroken chromosoom waardoor de cel stopt met delen of dood gaat.

 

 

De lengte van de telomeren worden met het ouder worden steeds iets minder, maar

de telomeerlengte wordt tevens be´nvloed door oxidatie/nitrosative stress en inflammatie.

 

 


 

 

Telomere length analysis in chronic fatigue syndrome.

The FASEB Journal. 2016 Apr; 30(Suppement 1): lb459.

Unger ER, Murray J, Oakley LP, Lin JM, Rajeevan MS.

 

 

Abstract

 

Background

 

Chronic fatigue syndrome (CFS)

is a severely disabling condition associated with multi-system symptoms

including marked post-exertional malaise, fatigue, pain, unrefreshing sleep and cognitive impairment.

 

The symptoms and risk factors share features with accelerating aging.

 

Aging and

a variety of metabolic, inflammatory, infectious and neoplastic conditions

have been associated with accelerated telomere attrition.

 

This analysis was performed to evaluate whether CFS shares this association.

 

 

Methods

 

DNA was isolated from 705 PAXgene whole blood samples

from 751 participants

in the 2007-09 follow-up of the Georgia CFS Surveillance study

who completed the clinical evaluation

used to identify exclusionary medical and psychiatric conditions

that could explain fatigue.

 

Using the 1994 CFS Research Case Definition

with questionnaire-based subscale thresholds for

fatigue, function and symptoms,

participants were classified as:

  1. CFS
  2. if all criteria met (n=71);

  3. CFS-X
  4. if CFS with exclusionary conditions (n=78);

  5. Insufficient Symptoms/Fatigue (ISF)
  6. if only some criteria met, regardless of exclusionary conditions (n=340);

  7. Non-Fatigued (NF)
  8. if no criteria met and no exclusionary conditions (n=212);

    47 NF participants with exclusions were not included and 3 could not be classified).

Relative telomere length was measured using real-time PCR.

 

Telomere specific primers generate a signal

proportional to total sum of the length of all telomeres in the sample (T).

 

Telomere signal is normalized to signal from primers to single-copy gene (S).

 

The T/S ratio is proportional to average telomere length per cell.

 

T/S is expressed relative to reference DNA, assigned T/S of 1.0.

 

Conversion of T/S to Southern blot hybridization determination of

terminal restriction fragment telomere length in base pairs (bp)

was based on data from 20 healthy volunteers tested by both methods.

 

Linear and logistic models were used

to examine association between CFS, T/S ratio and covariates.

 

Level of significance was set at p < 0.05.

 

This analysis concerned 639 participants with telomere, classification and co-variate data:

77 CFS-X, 64 CFS, 302 ISF, and 196 NF.

 

 

Results

 

Age (48.04 ▒ 0.38 years) did not differ across groups,

but obesity, sex, race, education and income, significantly differed.

 

T/S ratios ranged from 0.269 to 4.138.

 

When comparing T/S ratios across groups,

telomere lengths were significantly shorter in CFS and ISF than NF

(CFS: 0.93▒0.03, ISF: 0.94▒0.02; NF: 1.09▒0.04).

 

These differences remained significant

after adjusting for covariates (age, BMI, waist-hip-ratio, education, and sex).

 

Based on adjusted group means,

telomere length was shorter by 212, 593 and 508 bp in CFS-X, CFS and ISF compared to NF.

 

As expected there was

a significant negative correlation between telomere length and age in the study sample overall.

 

NF subjects started with long telomeres but shortened at a faster rate (59 bp/year)

than the rate of telomere shortening in CFS-X (25.4 bp/year), CFS (21.2 bp/year) and ISF (4.2 bp/year).

 

 

Conclusions

 

Our results indicate that

CFS should be included in the list of conditions associated with telomere shortening.

 

Further work is needed to evaluate if the shortening has functional significance in CFS.

 

 

Footnotes

 

This abstract is from the Experimental Biology 2016 Meeting.

 

There is no full text article associated with this abstract published in The FASEB Journal.

 

 

http://www.fasebj.org/content/30/1_Supplement/lb459.abstract

 

 


 

Met dank een Manja, die het internet beter inde gaten houdt dan ik.