Whats the difference between a drum machine and a neurologist…..You only have to punch the information into a drum machine once!
This study says that if you look at someone who gets HSCT, that they suffer nerve damage as evidenced by a release of nerve proteins.
They say “the Canadian regimen is considered particularly intensive and involves high‐dose cyclophosphamide and busulfan as conditioning agents. These drugs are selected not only for their peripheral myeloablative and lymphoablative actions but also for their CNS penetrance and toxicity to microglia involved in MS pathogenesis……Now I have to ask what is the evidence for any influence of cyclophosphamide on microglia? Cyclophosphamide are only going to work on proliferating cells and the literature if anything says its effect is to activates microglia….Anyway they wonder if the early effect of brain volume loss seen on MRI relates to nerve loss. ProfG and sort of gave the answer to this question ten years ago but they used a different way to to the ablation They said the process resulted in nerve damage. With time you reap the benefit of this “cruel to be kind approach”. So you ask why is progress so slow? Well “speculation” is the stake/light/garlic to the vampire and it makes people say you haven’t shown this, so you have to prove it agian and again and again.
Neurotoxicity after hematopoietic stem cell transplant in multiple sclerosis. Thebault S, Lee H, Bose G, Tessier D, Abdoli M, Bowman M, Berard J, Walker L, Rush CA, MacLean H, Booth RA, Narayanan S, Arnold DL, Tabard-Cossa V, Atkins HL, Bar-Or A, Freedman MS. Ann Clin Transl Neurol. 2020 Apr 18. doi: 10.1002/acn3.51045. [Epub ahead of print]
Accelerated brain volume loss has been noted following immunoablative autologous hematopoietic stem cell transplantation (IAHSCT) for multiple sclerosis. As with other MS treatments, this is often interpreted as ‘pseudoatrophy’, related to reduced inflammation. Treatment-related neurotoxicity may be contributory. We sought objective evidence of post-IAHSCT toxicity by quantifying levels of Neurofilament Light Chain (sNfL) and Glial Fibrillary Acidic Protein (sGFAP) before and after treatment as markers of neuroaxonal and glial cell damage.
Sera were collected from 22 MS patients pre- and post-IAHSCT at 3, 6, 9, and 12 months along with 28 noninflammatory controls. sNfL and sGFAP quantification was performed using the SiMoA single-molecule assay.
Pre-IAHSCT levels of sNfL and sGFAP were elevated in MS patients compared with controls (geometric mean sNfL 21.8 vs. 6.4 pg/mL, sGFAP 107.4 vs. 50.7 pg/mL, P = 0.0001 for both). Three months after IAHSCT, levels of sNfL and sGFAP increased from baseline by 32.1% and 74.8%, respectively (P = 0.0029 and 0.0004). sNfL increases correlated with total busulfan dose (P = 0.034), EDSS score worsening at 6 months (P = 0.041), and MRI grey matter volume loss at 6 months (P = 0.0023). Subsequent NfL levels reduced to less than baseline (12-month geometric mean 11.3 pg/mL P = 0.0001) but were still higher than controls (P = 0.0001). sGFAP levels reduced more slowly but at 12 months were approaching baseline levels (130.7 pg/mL).
There is direct evidence of transient CNS toxicity immediately after IAHSCT which may be chemotherapy mediated and contributes to transient increases in MRI atrophy.