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Saturday, May 17, 2008
Champagne Terrace/Bordeaux (Novotel London West)
Background:
Neuropathological and imaging studies in autism have shown abnormalities in neuronal-cortical organization as well as neuroinflammation. Because lipidomic analysis of tissues may provide evidence of abnormalities in lipid composition as well as oxidative stress as result of structural and neuroimmune reactions.
Objectives:
To determine the presence of abnormal patterns of lipid composition and oxidative stress in brain tissues obtained from patients with autism as compared with neurologically normal controls.
Methods:
Global lipid levels were obtained using a Sciex API 3,000 triple stage quadrupole tandem mass spectrometer (ESI/MS/MS) from fresh frozen brain tissues in patients with autism and controls obtained from the Autism Tissue Project. Brain samples from the frontal and occipital lobes (cerebral cortex, subcortical white matter, deep white matter) and cerebellum (folia and deep white matter) were available from 7 patients with autism and age-matched controls (n=9).
Results:
When brain sections of autistic patients were directly compared with normal controls the most significant changes were seen in the deep white matter of the frontal lobe. In this brain region, several species of ceramides (C16:0, C18:0 and C22:0), 4-hydroxynonenal (lysine and histidine), Vitamin E, and cholesterol (monomer and dimmer) were found to be elevated in autistic patients compared to controls. Interestingly, analysis of brain regions when we eliminated interpatient variation by using the occipital lobe of patients with autism as an internal control uncovered subtler changes in lipid levels such as a frontal lobe increases in cholesterol esters (palmatate and linoleate) within the deep white matter and increases of short chain sphingomyelin species (C18, C20, C22) in the cortex.
Conclusions:
Brain lipid alterations in autism may allude to three pathogenic mechanisms 1) increase oxidative stress and physiological compensation 2) deregulation of sterol metabolism and 3)possible alteration in packing density within the frontal lobe.
Neuropathological and imaging studies in autism have shown abnormalities in neuronal-cortical organization as well as neuroinflammation. Because lipidomic analysis of tissues may provide evidence of abnormalities in lipid composition as well as oxidative stress as result of structural and neuroimmune reactions.
Objectives:
To determine the presence of abnormal patterns of lipid composition and oxidative stress in brain tissues obtained from patients with autism as compared with neurologically normal controls.
Methods:
Global lipid levels were obtained using a Sciex API 3,000 triple stage quadrupole tandem mass spectrometer (ESI/MS/MS) from fresh frozen brain tissues in patients with autism and controls obtained from the Autism Tissue Project. Brain samples from the frontal and occipital lobes (cerebral cortex, subcortical white matter, deep white matter) and cerebellum (folia and deep white matter) were available from 7 patients with autism and age-matched controls (n=9).
Results:
When brain sections of autistic patients were directly compared with normal controls the most significant changes were seen in the deep white matter of the frontal lobe. In this brain region, several species of ceramides (C16:0, C18:0 and C22:0), 4-hydroxynonenal (lysine and histidine), Vitamin E, and cholesterol (monomer and dimmer) were found to be elevated in autistic patients compared to controls. Interestingly, analysis of brain regions when we eliminated interpatient variation by using the occipital lobe of patients with autism as an internal control uncovered subtler changes in lipid levels such as a frontal lobe increases in cholesterol esters (palmatate and linoleate) within the deep white matter and increases of short chain sphingomyelin species (C18, C20, C22) in the cortex.
Conclusions:
Brain lipid alterations in autism may allude to three pathogenic mechanisms 1) increase oxidative stress and physiological compensation 2) deregulation of sterol metabolism and 3)possible alteration in packing density within the frontal lobe.