Axonal damage induced by cerebrospinal fluid from patients with relapsing-remitting multiple sclerosis

  title={Axonal damage induced by cerebrospinal fluid from patients with relapsing-remitting multiple sclerosis},
  author={Alberto Alc{\'a}zar and Ignacio Regidor and Jaime Masju{\'a}n and Matilde Salinas and Jos{\'e} C. {\'A}lvarez-cerme{\~n}o},
  journal={Journal of Neuroimmunology},

Disturbed Glucose Metabolism in Rat Neurons Exposed to Cerebrospinal Fluid Obtained from Multiple Sclerosis Subjects

It is suggested that MS appears to be linked with metabolic deformity through hitherto unknown factors present in cerebrospinal fluid that may regulate axonal damage, remyelinate the axon and make functional recovery possible.

Bioenergetic Failure in Rat Oligodendrocyte Progenitor Cells Treated with Cerebrospinal Fluid Derived from Multiple Sclerosis Patients

The findings revealed downregulated expression of genes involved in carbohydrate metabolism, and that glucose metabolism impairment and reduced ATP availability for cellular damage repair clearly differentiate more benign forms from the most aggressive forms and worst prognosis in MS patients.

Neuronal and BBB damage induced by sera from patients with secondary progressive multiple sclerosis.

It is reported that the serum from patients with secondary progressive multiple sclerosis (SPMS) has a damaging effect on isolated neurons, suggesting that neuronal damaging in MS could be a primary event and not only secondary to myelin damage, as generally assumed.

Cerebrospinal fluid ceramides from patients with multiple sclerosis impair neuronal bioenergetics.

The data suggest that C16:0 and C24:0 ceramides are enriched in the cerebrospinal fluid of patients with multiple sclerosis and are sufficient to induce neuronal mitochondrial dysfunction and axonal damage.

Cryptic Axonal Antigens and Axonal Loss in Multiple Sclerosis

Evidence that antibodies to axolemma-enriched fractions (AEF) isolated from CNS myelinated axons may play a role in axonal destruction is summarized and it is proposed that these AEF antigens are cryptic because they are shielded from immune surveillance in vivo via the tightly sealed paranodal loops of myelin.



Blood‐Brain Barrier Abnormalities in Longstanding Multiple Sclerosis Lesions. An Immunohistochemical Study

  • E. KwonJ. Prineas
  • Biology, Medicine
    Journal of neuropathology and experimental neurology
  • 1994
The findings suggest that the blood-brain barrier (BBS) is permanently damaged in many old plaques, although to a degree not often detectable by current gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI).

Axonal damage in acute multiple sclerosis lesions.

The results show the expression of amyloid precursor protein in damaged axons within acute multiple sclerosis lesions, and in the active borders of less acute lesions, which may have implications for the design and timing of therapeutic intervention.

Axonal transection in the lesions of multiple sclerosis.

Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.

Imaging axonal damage of normal-appearing white matter in multiple sclerosis.

Results add to data suggesting that axonal damage or loss may be responsible for functional impairments in multiple sclerosis, and may be of particular significance for understanding chronic disability in this disease.

A gliotoxic factor and multiple sclerosis

1H magnetic resonance spectroscopy of chronic cerebral white matter lesions and normal appearing white matter in multiple sclerosis

The hypothesis that axonal loss is important in the development of disability in multiple sclerosis is supported and evidence for axonal Loss in normal appearing white matter in patients with primary progressive disease is provided.

Chemical pathology of acute demyelinating lesions and its correlation with disability

The results suggest that neuronal dysfunction may be a proximate mechanism of disability even in inflammatory disorders primarily affecting myelin and oligodendroglial cells.

Distinct Patterns of Multiple Sclerosis Pathology Indicates Heterogeneity in Pathogenesis

A new classification scheme of lesional activity on the basis of the molecular composition of myelin degradation products in macrophages is presented and it is indicated, that the demyelinated plaques of multiple sclerosis may reflect a common pathological end point of a variety of different immunological mechanisms ofMyelin destruction in this disease.