“…The present paper describes the pathomorphological findings in four outbreaks of leukoencephalomyelopathy in colonies of SPF cats fed irradiated dry cat food in the Netherlands between 1989 and 2001. Because a definite cause for the disease has not been established until now, and the demyelinating lesions and their distribution throughout the white matter of the central nervous system in these cats show resemblance to primary demyelination due to defective or improper myelin formation as in Canavan's disease and adreno‐myelopathy in man and associated experimental mouse models (Baumann & Pham‐Dinii, ); polyunsaturated fatty acids, including essential fatty acids (EFA), are highly vulnerable to irradiation due to an increase in lipid peroxide formation (Hammer & Wills, ), reflected by higher thiobarbituric acid reactive substances (TBARS) and nuclear magnetic resonance (NMR) values after irradiation (De Oliveira Silva, Mársico, Oliveira de Jesus, Guimarães, & Sloboda Cortez, ) mostly affecting polyunsaturated fatty acids resulting in more saturated fatty acids (Javan & Motallebi, ), and increased formation of trans fatty acids (Yilmaz & Geçgel, ); nervous tissue concentrates omega‐3 polyunsaturated fatty acids in myelin (Lenox, ); lipid composition and fatty acid profiles of myelin of rat brain vary in response to the consumption of different fats (Bourre et al, ; Srinivasarao, Vajreswari, Rupalatha, & Narayanareddy, ); and induction of EFA deficiency in rats resulted in both a decrease of EFA in myelin but also vacuolation/myelin splitting in the optic nerve (Trapp, ), we hypothesized that abnormalities in fatty acid metabolism in myelin might play an essential role in the pathogenesis of this acquired form of leukoencephalomyelopathy in cats. Therefore, we investigated in addition the fatty acid profile of the white matter of the spinal cord of affected cats and control animals, and of irradiated and non‐irradiated food.…”