- April 2018: CSF derived from PPMS delays remyelination. CSF taken from PPMS patients delays remyelination in mice.
- Dec. 2017: Disturbed glucose metabolism in Rat Neurons Exposed to CSF from MS. CSF from MS patients is toxic and kills rat neurons due to a glucose metabolism disturbation.
- Jul 2017: Bioenergetic Failure in Rat OPC treated with CSF from MS (OPC = Oligodendrocyte Progenitor Cells). CSF from MS patients is toxic and kills rat oligodrendrocytes.
- Jun 2017: Effect of EVs from CSF of MS patients and healthy controls on astrocytes in culture. Extracelular Vesicles (EVs) are waste remainings from cells, and are present in the CSF. In MS patients they are toxic to astrocytes.
-Jan. 2016: Effect of the Sera of Patients with MS on apoptosis and Nitric Oxide Production of Endothelial Cells. Not CSF but serum. Endothelial cells treated with serum of patients with MS die by apoptosis.
- Nov 2015: Quantified CSF antibody reactivity against myelin in MS. CSF from patients with MS have higher reactivity toward purified myelin particles as compared to those with OND with OCBs.
- Nov 2014: Progressive multiple sclerosis cerebrospinal fluid induces inflammatory demyelination, axonal loss, and astrogliosis in mice. Progresive MS can be passed from patients to mice via CSF injection.
- August 2014: Cerebrospinal fluid ceramides from patients with multiple sclerosis impair neuronal bioenergetics. A couple of substances called ceramides are enriched in the CSF of MS patients[/url] and are sufficient to induce neuronal mitochondrial dysfunction and axonal damage.
- August 2014: Tiwari-Woodruff SK1, Myers LW, Bronstein JM. Cerebrospinal fluid immunoglobulin G promotes oligodendrocyte progenitor cell migration. J Neurosci Res.
- April 2014: Development of Inflammatory Demyelinating Lesions In Mouse CNS After Injection Of Cerebrospinal Fluid Derived From Progressive MS Patients. CSF from MS patients is toxic and produces inflammatory demyelinating lesions in mice.
- June 2014: CSF ceramides from patients with MS impair neuronal bioenergetics. An observed toxic effect of cerebrospinal fluid on neurons was attributable to ceramides.
- 2013: CSF from PMS patients alters neural precursor cells growth: CSF from PPMS patients produce changes in CNS cells.
- : Detection of a gliotoxic activity in the CSF from MS patients. Cytotoxic activity reported in MS CSF.
Other previous reports:
* Feb. 2004: Cid C1, Alvarez-Cermeño JC, Camafeita E, Salinas M, Alcázar A. Antibodies reactive to heat shock protein 90 induce oligodendrocyte precursor cell death in culture. Implications for demyelination in multiple sclerosis FASEB J.
* Nov. 2002: Alvarez-Cermeño JC1, Cid C, Regidor I, Masjuan J, Salinas-Aracil M, Alcázar-González A. The effect of cerebrospinal fluid on neurone culture: implications in the pathogenesis of multiple sclerosis. Rev Neurol.
* Apr. 2000: Alcázar A1, Regidor I, Masjuan J, Salinas M, Alvarez-Cermeño JC. Axonal damage induced by cerebrospinal fluid from patients with relapsing-remitting multiple sclerosis, J Neuroimmunol.
*SPAG16: an autoantibody target in CSF and plasma of MS patients(http://www.researchgate.net/profile/Lau ... 53956e.pdf)
* some pictures of the CSF acting over a culture (http://www.ncbi.nlm.nih.gov/pmc/article ... re/d35e78/)
*Quantified CSF antibody reactivity against myelin in multiple sclerosis(http://onlinelibrary.wiley.com/doi/10.1 ... 3.264/full)
*May 2001 - Apoptosis in neurones exposed to cerebrospinal fluid from patients with multiple sclerosis or acute polyradiculoneuropathy, https://doi.org/10.1016/S0022-510X(01)00496-8, a significant increase in apoptosis was observed in cultures exposed to cerebrospinal fluid from patients with primary progressive multiple sclerosis, and apoptosis correlated with disease severity. This supports the existence of biochemical differences between subgroups of multiple sclerosis. A significant increase in apoptosis was also induced by cerebrospinal fluid samples from patients with acute polyradiculoneuropathy, suggesting the presence of neurotoxic factor(s) here also.
*February 1998: A gliotoxic factor and multiple sclerosis. https://doi.org/10.1016/S0022-510X(97)00231-1, 3-day exposure to heat-treated cerebrospinal fluid (CSF) from MS patients caused apoptotic death of astrocytes and oligodendrocytes
*Glial toxicity in urine and multiple sclerosis, https://journals.sagepub.com/doi/abs/10 ... 0100700607
*A urinary marker for multiple sclerosis: https://www.thelancet.com/journals/lanc ... 5/fulltext
Cerebrospinal Fluid Derived from Primary Progressive MS Delays Remyelination after Lysolecithin-induced Demyelination
https://tischms.org/research/published/ ... tion-after
Objective: To investigate whether primary progressive MS (PPMS) cerebrospinal fluid (CSF) impacts remyelination after lysolecithin-induced demyelination.
Background: In PPMS the clinical course is progressive from disease onset suggesting that remyelination is impaired in contrast to relapsing-remitting (RRMS) forms of the disease. To investigate this phenomenon we used the lysolecithin-induced demyelination model of the disease. In this model, remyelination spontaneously commences usually 7 days post lysolecithin administration. We studied whether factors present in CSF from PPMS patients would inhibit this remyelination.
Design/Methods: Mice underwent a laminectomy at cervical level 5 (C5) and 1μl of 1% lysolecithin was injected into the dorsal column. At 5 days post lysolecithin injection, 3μl cerebrospinal fluid from untreated PPMS patients was injected into the subarachnoid space also at C5. Control mice were injected with saline or CSF obtained from healthy individuals. Behavioral deficits were assessed at multiple time points post CSF administration. Mice were perfused 12 days after lysolecithin injection and pathology was assessed in the spinal cord.
Results: PPMS CSF-injected mice exhibited significantly impaired forelimb function and increased tail flaccidity compared to controls. Luxol fast blue staining revealed a significantly larger volume of demyelination in PPMS CSF-injected mice than mice injected with saline or healthy control CSF. Mice injected with PPMS CSF also showed a significant increase in microglial activation and an increase in reactive astrogliosis, as assessed by Iba-1 and GFAP immunostaining respectively. No significant change in the number of proliferating oligodendrocyte progenitor cells, as assessed by NG2 and Ki67, or mature oligodendrocytes, assessed by APC and Olig2, was observed.
Conclusions: Intrathecal delivery of PPMS CSF at the site of a lysolecithin-induced lesion yielded larger lesions, accompanied by increased microglial activation and reactive astrogliosis in the cervical spinal cord, as compared to controls. Identification of the CSF factors responsible for this delay in remyelination is an important next step.
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