Monday, 23 June 2014

Ageing in MS

What has ageing go to do with MS? Progression maybe. #MSBlog #MSResearch

"In most studies age is the most powerful predictor of the onset of progressive MS. The older you are the more likely you are to have progressive disease. Children with MS almost never present with progressive MS and the time to onset of SPMS is longer. Why? Some in the field hypothesise that it is due to a failure of reparative mechanisms that are age-related. Some of you who have children will know how quickly they repair cuts compared to their aged-parents. There is good data in from animals supporting this hypothesis; aged rats remyelinate lesions a lot slower than young rats. The study below suggests the same happens in MS lesions. White matter in MS lesions in young MSers had better MTR metrics than lesions from older MSers. MTR is marker of remyelination. Lesions in young MSers were more likely to be remyelinated."

"What can we do about ageing? Ageing is a physiological process and therefore it may prove to be druggable in the future. You are all aware of the recent experiments of sewing together the circulations of young and older mice, which resulted in improvements in brain functioning of the older mice. These so called parabiosis experiments tell us that there is some soluble factor in young mice that promotes repair and augments brain function in older mice. If we can identify this factor, or cocktail of factors, we may be able to treat the ageing MS brain and promote repair. Is this another bit of science fiction? No I don't think. In addition to animal experiments we see clinical examples of delayed ageing and accelerated ageing. Therefore ageing is a physiological process and we will almost certainly be able to manipulate these processes. I predict that we will see anti-ageing medications in my lifetime and they may benefit MSers."


"For those of you interested in evolutionary medicine will know that evolution built in senescence, or ageing, into biological systems for a reason. If we remove or delay ageing we may affect natural selection and the delicate balance that exists between new and old. This is why any treatments that prevent or delay ageing will have ethical and philosophical ramifications."

Newbould et al. Age independently affects myelin integrity as detected by magnetization transfer magnetic resonance imaging in multiple sclerosis. Neuroimage Clin. 2014 ;4:641-8.

BACKGROUND: MS is a heterogeneous disorder with a progressive course that is difficult to predict on a case-by-case basis. Natural history studies of MS have demonstrated that age influences clinical progression independent of disease duration.

OBJECTIVE: To determine whether age would be associated with greater CNS injury as detected by magnetization transfer MRI.

MATERIALS AND METHODS: 40 MSers were recruited from out-patient clinics into two groups stratified by age but with similar clinical disease duration as well as 13 controls age-matched to the older MS group. Images were segmented by automated programs and blinded readers into normal appearing white matter (NAWM), normal appearing gray matter (NAGM), and white matter lesions (WMLs) and gray matter lesions (GMLs) in the MS groups. WML and GML were delineated on T2-weighted 3D fluid-attenuated inversion recovery (FLAIR) and T1 weighted MRI volumes. Mean magnetization transfer ratio (MTR), region volume, as well as MTR histogram skew and kurtosis were calculated for each region.

RESULTS: All MTR measures in NAGM and MTR histogram metrics in NAWM differed between MS subjects and controls, as expected and previously reported by several studies, but not between MS groups. However, MTR measures in the WML did significantly differ between the MS groups, in spite of no significant differences in lesion counts and volumes.

CONCLUSIONS: Despite matching for clinical disease duration and recording no significant WML volume difference, we demonstrated strong MTR differences in WMLs between younger and older MS patients. These data suggest that aging-related processes modify the tissue response to inflammatory injury and its clinical outcome correlates in MS.

4 comments:

  1. "For those of you interested in evolutionary medicine will know that evolution built in senescence, or ageing, into biological systems for a reason. If we remove or delay ageing we may affect natural selection and the delicate balance that exists between new and old. This is why any treatments that prevent or delay ageing will have ethical and philosophical ramifications."

    I think this comment - particularly including the last sentence - could be misinterpreted as questioning interventions that extend people's life span. Humans, of course, have interferred with 'natural selection' ever since trepanning and herbalism were used to make their tribal fellows better (and perhaps live longer) right up to our age of intensive care units, genomics, antibiotics and disease modifying drugs. I doubt trying to alter the process of senescence on a molecular level is of fundamental difference here. Do your concerns rather refer to specific experiments that people may wonder could go too far if applied to humans (e.g. breaking boundaries between individuals and/or between mice and men)?

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    1. I am not arguing against treating disease. The philosophical question I am asking Is age a disease? If it is how do we define it and how do we treat it. A disease is a clinicopathological entity that can be defined conventionally or using pre-theoretical or theoretical contructs. Making ageing a disease questions our evolutionary history and changes the way we look at life. Some food for thought.

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  2. The best solution is to freeze your head until a cure is found and impant your cured brain in a young body.

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  3. okay sounds good would you like your new body? life is to be lived for not to be envy for ;-)

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