Changes in dietary folate intake differentially affect oxidised lipid and mitochondrial DNA damage in various brain regions of rats in the absence/presence of intracerebroventricularly injected amyloid ß-peptide challenge.

Accumulating evidence suggests that changes in dietary folate intake may modulate the risks of Alzheimer's disease (AD) through as yet unknown mechanisms. The aims of the present study were to investigate how dietary folate affects the brain folate distribution, levels of oxidised lipid and DNA damage in the absence/presence of ß-amyloid(25-35) (Aß) peptide challenge, a pathogenic hallmark of AD. Male Wistar rats were assigned to diets with folic acid at 0 (folate deprivation; FD), 8 (moderate folate; MF) and 8 mg folic acid/kg diet+0·003 % in drinking-water (folate supplementation; FS) for 4 weeks. A single injection of Aß peptide (1 mg/ml) or the vehicle solution was intracerebroventricularly (icv) administrated to rats a week before killing. Brain folate, a marker of oxidative injury, and neuronal death were assayed. In the absence of an Aß injection, FD rats showed reduced folate levels, and increased 2-thiobarbituric acid-reactive substances and a mitochondrial (mt)DNA 4834 bp large deletion (mtDNA4834 deletion) in the hippocampus compared with the counterpart brains of control rats (P < 0·05). A single icv injection of Aß peptide potentiated lipid peroxidation in the medulla of FD rats, which was ameliorated by feeding FD rats with the MF and FS diets (P < 0·05). Feeding the FS diet to Aß-injected rats enriched brain folate levels and reduced mtDNA4834 deletion in the hippocampal and medullary regions compared with corresponding tissues of Aß+FD rats (P < 0·05). Aß+FS rats had reduced rates of neuronal death in the frontal cortex compared with Aß+FD rats (P < 0·05). Taken together, our data revealed that folate deprivation differentially depleted brain folate levels, and increased lipid peroxidation and mtDNA4834 deletions, particularly, in the hippocampus. Upon Aß challenge, the FS diet may protect various brain regions against lipid peroxidation, mitochondrial genotoxicity and neural death associated with folate deprivation.

Estimation of prevalence and incidence of infantile spasms in Taiwan using capture-recapture method.

PURPOSE: To estimate the prevalence, incidence, and case-fatality of infantile spasms (IS) in Taiwan. METHODS: A retrospective cohort of patients with IS was obtained from one medical center to identify 69 IS cases from 1985 to 1997. This cohort, in conjunction with the claimed data from the National Health Insurance, was used to estimate the prevalence and incidence of IS by capture-recapture design, taking the case-fatality of IS into account. RESULTS: The prevalence rate of IS for aged 0-9 years was 0.046 per thousand. The incidence rate was estimated as 6 over 100,000 per year in Taiwan. Of the 69 IS cases, 8 deaths were ascertained. The case-fatality rate was 11.6%. The leading cause of death was status epilepticus. CONCLUSIONS: We have demonstrated an efficient method to estimate the incidence and prevalence rates of IS in Taiwan. Our results help to make a clear understanding of the disease burden of IS in this society.