Gray matter atrophy

A board to discuss the newly-released drug Tysabri, (formerly known as Antegren) as a treatment for Multiple Sclerosis
Post Reply
User avatar
Petr75
Family Elder
Posts: 222
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Has thanked: 1 time
Been thanked: 2 times

Gray matter atrophy

Post by Petr75 » Fri Jan 11, 2019 1:08 pm

2018 Dec 21
Division of Clinical Neurosciences, Turku University Hospital and University of Turku, Turku, Finland.
Department of Neurology, Oregon Health Science University, Portland, Oregon, United States of America ..
Gray matter atrophy in multiple sclerosis despite clinical and lesion stability during natalizumab treatment.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6303064/

Abstract
BACKGROUND:
Brain volume loss is an important surrogate marker for assessing disability in MS; however, contribution of gray and white matter to the whole brain volume loss needs further examination in the context of specific MS treatment.
OBJECTIVES:
To examine whole and segmented gray, white, thalamic, and corpus callosum volume loss in stable patients receiving natalizumab for 2-5 years.
METHODS:
This was a retrospective study of 20 patients undergoing treatment with natalizumab for 24-68 months. Whole brain volume loss was determined with SIENA. Gray and white matter segmentation was done using FAST. Thalamic and corpus callosum volumes were determined using Freesurfer. T1 relaxation values of chronic hypointense lesions (black holes) were determined using a quantitative, in-house developed method to assess lesion evolution.
RESULTS:
Over a mean of 36.6 months, median percent brain volume change (PBVC) was -2.0% (IQR 0.99-2.99). There was decline in gray (p = 0.001) but not white matter (p = 0.6), and thalamic (p = 0.01) but not corpus callosum volume (p = 0.09). Gray matter loss correlated with PBVC (Spearman's r = 0.64, p = 0.003) but not white matter (Spearman's r = 0.42, p = 0.07). Age significantly influenced whole brain volume loss (p = 0.010, multivariate regression), but disease duration and baseline T2 lesion volume did not. There was no change in T1 relaxation values of lesions or T2 lesion volume over time. All patients remained clinically stable.
CONCLUSIONS:
These results demonstrate that brain volume loss in MS is primarily driven by gray matter changes and may be independent of clinically effective treatment.
https://www.ncbi.nlm.nih.gov/pubmed/30576361

vesta
Family Elder
Posts: 589
Joined: Thu Jul 12, 2012 9:10 am
Location: Paris, France
Been thanked: 3 times
Contact:

Re: Gray matter atrophy

Post by vesta » Wed Jan 16, 2019 3:08 am

Petr75 wrote:
Fri Jan 11, 2019 1:08 pm
2018 Dec 21
Division of Clinical Neurosciences, Turku University Hospital and University of Turku, Turku, Finland.
Department of Neurology, Oregon Health Science University, Portland, Oregon, United States of America ..
Gray matter atrophy in multiple sclerosis despite clinical and lesion stability during natalizumab treatment.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6303064/

Abstract
BACKGROUND:
Brain volume loss is an important surrogate marker for assessing disability in MS; however, contribution of gray and white matter to the whole brain volume loss needs further examination in the context of specific MS treatment...
OBJECTIVES:
To examine whole and segmented gray, white, thalamic, and corpus callosum volume loss in stable patients receiving natalizumab for 2-5 years.
METHODS:
This was a retrospective study of 20 patients undergoing treatment with natalizumab for 24-68 months. Whole brain volume loss was determined with SIENA. Gray and white matter segmentation was done using FAST. Thalamic and corpus callosum volumes were determined using Freesurfer. T1 relaxation values of chronic hypointense lesions (black holes) were determined using a quantitative, in-house developed method to assess lesion evolution.
RESULTS:
Over a mean of 36.6 months, median percent brain volume change (PBVC) was -2.0% (IQR 0.99-2.99). There was decline in gray (p = 0.001) but not white matter (p = 0.6), and thalamic (p = 0.01) but not corpus callosum volume (p = 0.09). Gray matter loss correlated with PBVC (Spearman's r = 0.64, p = 0.003) but not white matter (Spearman's r = 0.42, p = 0.07). Age significantly influenced whole brain volume loss (p = 0.010, multivariate regression), but disease duration and baseline T2 lesion volume did not. There was no change in T1 relaxation values of lesions or T2 lesion volume over time. All patients remained clinically stable.
CONCLUSIONS:
These results demonstrate that brain volume loss in MS is primarily driven by gray matter changes and may be independent of clinically effective treatment.
https://www.ncbi.nlm.nih.gov/pubmed/30576361
Thanks for posting this excellent article. Besides the drug being in itself dangerous, it doesn't "work" if grey matter atrophy continues, therefore potential handicap. Time to forget the drug approach and consider the CNS fluid circulation pathology in MS.

Best regards, Vesta

User avatar
Petr75
Family Elder
Posts: 222
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic
Has thanked: 1 time
Been thanked: 2 times

Re: Gray matter atrophy

Post by Petr75 » Wed Jan 23, 2019 8:13 am

2018 Feb 15
Department of Biofunctional Imaging, Preeminent Medical Photonics Education & Research Center, Hamamatsu University School of Medicine, Hamamatsu, Japan
Neuroinflammation following disease modifying therapy in multiple sclerosis: A pilot positron emission tomography study.
https://www.ncbi.nlm.nih.gov/pubmed/29406909

Abstract
INTRODUCTION:
Chronic activation of microglia accelerates the neurodegenerative process in multiple sclerosis (MS). Although disease modifying therapy (DMT) is reportedly effective for neuroinflammatory responses in MS, the progression of neuroinflammation after DMT remains unclear.
METHODS:
We evaluated microglial activation in six clinically stable relapsing-remitting MS patients after DMT by quantifying changes in translocator protein (TSPO) density using PET with [11C]DPA713, a selective TSPO tracer for microglial activation. All patients underwent [11C]DPA713 PET scans twice, and the scans were conducted one year apart. The binding potential (BPND) of the tracer was estimated using a simplified reference tissue model.
RESULTS:
[11C]DPA713 BPND measured at 6months after DMT was significantly higher in the MS group than that in the control group. Compared with the first PET measurement, the one-year PET measurement revealed significantly elevated [11C]DPA713 BPND in broader brain regions covering the temporal and parietal cortices after one year of DMT.
CONCLUSIONS:
The current results indicate that microglial activation may proceed in the entire brain of clinically stable MS patients even after receiving DMT.

Post Reply
  • Similar Topics
    Replies
    Views
    Last post