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MOTOR NEURON DISEASE

Defects in adenosine metabolism identified in ALS

Nature Reviews Neurology volume 15, page 127 (2019)Cite this article

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Patients with amyotrophic lateral sclerosis (ALS) — a motor neuron disease (MND) characterized by degeneration of upper and lower motor neurons — exhibit dysfunctional energy metabolism, which is known to contribute to disease progression. In a new study published in Brain, Scott Allen and colleagues have pinpointed a specific ALS-associated defect in astrocytic adenosine metabolism that could be amenable to therapeutic intervention.

“We previously found that in patients with ALS, skin cells showed similar mitochondrial defects to CNS cells, such as neurons and astrocytes,” explains Allen. “However, unlike CNS cells, skin cells could upregulate their glycolytic pathways to maintain energy levels, and this started me thinking about the intrinsic ability of different cell types to mobilize alternative energy supplies to cope with bioenergetic stress — a property that I have termed ‘metabolic flexibility’.”

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Further reading

  • Allen, S. P. et al. Superoxide dismutase 1 mutation in a cellular model of amyotrophic lateral sclerosis shifts energy generation from oxidative phosphorylation to glycolysis. Neurobiol. Aging 35, 1499–1509 (2014)

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  1. Nature Reviews Neurology http://www.nature.com/nrneurol/

    Heather Wood

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  1. Heather Wood
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Correspondence to Heather Wood.

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Wood, H. Defects in adenosine metabolism identified in ALS. Nat Rev Neurol 15, 127 (2019). https://doi.org/10.1038/s41582-019-0147-7

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