Research press release


Nature Medicine

Reversible axon damage in multiple sclerosis



今回、M Kerschensteinerらは、生きたマウスの画像化を行い、多発性硬化症の実験モデルにおいて、新しい形態の軸索損傷を発見した。この疾患過程は、「局所的軸索変性(FAD)」と呼ばれ、軸索内ミトコンドリアの局部損傷、神経繊維の腫大、その後の軸索の断片化という各段階が順番に発生する。この実験では、ほとんどの腫大した軸索は、数日間にわたって状態に変化が見られず、その一部は自然に回復した点が注目に値する。


Axon damage might be spontaneously reversible in multiple sclerosis, according to research published online this week in Nature Medicine.

In multiple sclerosis, an inflammatory disease of the central nervous system, immune-mediated axon damage leads to permanent neurological deficits. How axon damage is initiated is not known. A classical view of multiple sclerosis is that loss of myelin ― the sheath that insulates axons to speed up the transmission of nerve signals ― is a prerequisite for axon damage.

Martin Kerschensteiner and his colleagues used imaging techniques in live mice to identify a new form of axon damage in an experimental model of multiple sclerosis. This process, termed ‘focal axonal degeneration’ (FAD), consists of sequential stages: localized damage to mitochondria within the axons, swellings of the nerve fiber and subsequent axon fragmentation. Notably, most swollen axons in their experiments persisted unchanged for several days, and some recovered spontaneously.

The team also found axonal changes consistent with FAD in lesions from patients with multiple sclerosis, highlighting the potential relevance of this form of axonal damage to the human disease.

doi: 10.1038/nm.2324


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