Acta Neuropathol Commun June 2023 PMID 37331971

Abcd1 deficiency accelerates cuprizone-induced oligodendrocyte loss and axonopathy in a demyelinating mouse model of X-linked adrenoleukodystrophy.

Ksenija Martinović, Jan Bauer, Markus Kunze, Johannes Berger, Sonja Forss-Petter

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Abstract in brief

Abcd1 deficiency in a mouse model of X-linked adrenoleukodystrophy (XALD) increases vulnerability of mature oligodendrocytes and causes more axonal damage during cuprizone-induced demyelination, suggesting a primary role of oligodendrocytes in disease pathology.
The study found that the absence of ABCD1 leads to accumulation of very long-chain fatty acids, which heightens the susceptibility of oligodendrocytes to cell death and nerve fiber damage during demyelination, without significantly altering microglial activity or the capacity for remyelination.
These results imply that oligodendrocyte loss and axonal injury in XALD may be directly linked to cell-autonomous effects of VLCFA buildup, rather than inflammatory processes or microglial dysfunction, highlighting potential targets for therapeutic intervention.]

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ABCD1 Deficiency Exacerbates Oligodendrocyte Loss and Axon Damage in Demyelination Model

ABCD1 deficiency in a mouse model of X-linked adrenoleukodystrophy increases vulnerability of oligodendrocytes and causes more axonal damage during cuprizone-induced demyelination. The absence of ABCD1 leads to fatty…

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New from #FWFOpenAccess https://t.co/ORPsZjIJLe Abcd1 deficiency accelerates cuprizone-induced oligodendrocyte loss and axonopathy in a demyelinating mouse model of X-linked adrenoleukodystrophy.

Jun 21, 2023 · 1,553 followers View post →