Review article

https://doi.org/10.2478/v10004-007-0029-z

Axonal Degeneration and Neuropathy Target Esterase

Paul Glynn

Abstract

This brief review summarises recent observations which suggest a possible mechanism for organophosphateinduced delayed neuropathy (OPIDN). Neuropathy target esterase (NTE) has been shown to deacylate endoplasmic reticulum (ER) membrane phosphatidylcholine (PtdCho). Raised levels of PtdCho are present in the brains of swiss cheese/NTE mutant Drosophila together with abnormal membrane structures, axonal and dendritic degeneration and neural cell loss. Similar vacuolated pathology is found in the brains of mice with brain-specific deletion of the NTE gene and, in old age, these mice show clinical and histopathological features of neuropathy resembling those in wild-type mice chronically dosed with tri-ortho-cresylphosphate. It is suggested that OPIDN results from the loss of NTE’s phospholipase activity which in turn causes ER malfunction and perturbation of axonal transport and glial-axonal interactions.

Keywords

brain; carbamate; endoplasmic reticulum; organophosphate; phospholipid

Hrčak ID:

16535

URI

https://hrcak.srce.hr/16535

Publication date:

26.9.2007.

Article data in other languages: croatian

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