We evaluated the activities of carnitine palmitoyltransferase (CPT), carnit
ine octanoyltranferase (COT), and carnitine acetyltransferase (CAT) in the
frontal cortex, temporal cortex, parietal cortex, hippocampus, and cerebell
um of Alzheimer disease (AD) patients and normal human brains. There were n
o significant differences in total CPT activity, its inhibition by malonyl-
CoA, the effect of the detergent Triton X-100 on CPT activity, COT activity
, and CAT activity in any of the brain regions examined, whether activities
were expressed as grams of wet weight or corrected for noncollagen protein
content. The addition of Triton X-100 increased CAT activity by 50%. Our r
esults suggest that there is no defect of fatty acid transport within the A
D brain cell. Total CPT activity, COT activity, and CAT activity are not af
fected in AD nor is the ratio of CPT I to CPT II altered in the AD versus t
he normal human brain.