Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8478393 | Molecular and Cellular Neuroscience | 2018 | 40 Pages |
Abstract
It is hypothesized that the observed Cu accumulations may represent a pathologic feature of ALS, which may actively contribute to axonal retraction leading to muscular denervation, and possibly significantly contributing to disease pathology. Therefore, it is proposed that the toxic-gain-of-function and dying-back hypotheses to explain the molecular drivers of ALS may not be separate, individual processes; rather our data suggests that they are parallel processes.
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Authors
T. Gabriel Enge, Heath Ecroyd, Dianne F. Jolley, Justin J. Yerbury, Bernadett Kalmar, Anthony Dosseto,