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Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Mitochondrial Membranes01:45

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Alterations in Muscle Tone lll01:11

Alterations in Muscle Tone lll

Rigidity and myotonia are distinct abnormalities of muscle tone that affect resistance and relaxation during movement. Although both involve altered muscle contraction, they arise from different neurological and muscular mechanisms.CharacteristicsRigidity is characterized by uniform resistance to passive movement across the entire range, independent of speed, affecting flexors and extensors equally. It may appear as lead-pipe rigidity (smooth, constant resistance) or cogwheel rigidity...

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Updated: May 22, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

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Published on: July 19, 2019

Mitochondrial changes within axons in multiple sclerosis: an update.

Graham R Campbell1, Nobuhiko Ohno, Doug M Turnbull

  • 1Centre for Neuroregeneration, University of Edinburgh, Chancellor's Building, Edinburgh, UK.

Current Opinion in Neurology
|May 1, 2012
PubMed
Summary
This summary is machine-generated.

Axonal mitochondria increase after demyelination in multiple sclerosis (MS) and experimental models. This increase persists after remyelination, suggesting potential therapeutic targets for progressive MS.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Multiple Sclerosis (MS) pathogenesis involves an energy-deficient state.
  • Axons in the central nervous system rely on mitochondria for energy, primarily located in juxtaparanodal and internodal regions.
  • The myelin sheath, axonal mitochondria, and electrogenic machinery form a critical triad disrupted in MS.

Purpose of the Study:

  • To review recent developments in axonal mitochondrial responses to demyelination and remyelination in multiple sclerosis.
  • To examine mitochondrial changes following experimental demyelination and myelination.

Main Methods:

  • Review of existing literature on axonal mitochondrial response in MS and experimental models.
  • Analysis of studies investigating mitochondrial content and distribution in demyelinated and remyelinated axons.

Main Results:

  • Axonal mitochondrial content significantly increases following demyelination in MS and experimental models.
  • Elevated axonal mitochondrial content persists even after the inflammatory response subsides.
  • Remyelination does not restore axonal mitochondrial content to levels observed in healthy, myelinated axons.

Conclusions:

  • Understanding the mechanisms behind axonal mitochondrial adaptation to myelin damage is crucial.
  • Investigating whether these mitochondrial responses are beneficial could reveal therapeutic targets for progressive MS.