Objectives
To evaluate pregnancy outcomes in Japanese patients with multiple sclerosis (MS) enrolled in a postmarketing surveillance study of intramuscular interferon beta‐1a (IM IFN beta‐1a).
Methods
Safety data were collected from Japanese patients receiving 30 μg weekly IM IFN beta‐1a. Pregnancy outcomes and annualized relapse rates (ARR) were analyzed retrospectively in patients who registered into the postmarketing surveillance study.
Results
A total of 1110 of 1638 patients registered in the postmarketing surveillance study were women. A total of 21 pregnancies (20 patients) resulted in 17 live births, 2 induced abortions, one spontaneous abortion and one unknown outcome. Weights and lengths of the 17 newborns were similar to newborns in the general Japanese population. No complications or malformations were reported. Of these 20 patients, nine experienced relapses in the year after childbirth, two experienced relapses in the year before pregnancy, and one experienced relapses before and during pregnancy. The mean (standard deviation) ARR was 0.94 (2.18) in the year before pregnancy, 0.25 (1.00), 0 (0) and 0 (0) in the three trimesters of pregnancy, and 1.05 (1.81), 0.84 (1.68), 0.63 (2.01) and 0.21 (0.92) in the first four quarters postpartum. Of the five patients who relapsed during the first quarter postpartum, only one had resumed IFN beta‐1a treatment for 35 days.
Conclusions
Although sample size limits our ability to draw definitive conclusions, we did not find evidence that IFN beta‐1a has adverse effects on pregnancy outcomes in Japanese patients with MS. Early IFN beta‐1a resumption might reduce the risk of relapse within the first quarter postpartum.
The main pathogenesis of Alzheimer's disease (AD) is related to the accumulation of amyloid-b (Ab) peptides in the brain that leads to neuronal cell death. In this study, we identified compounds in a methanol extract of the fruiting body of Polyozellus multiplex that inhibited Ab aggregation and are neuroprotective.Seven compounds against Ab40 aggregation were obtained through bioactivityguided fractionation of the extract, including polyozellin (1), kynapcin-12 (2), NSC617425 (3), cycloleucomelone (4), Bl-V (5), succinic acid (6), and protocatechuic acid (7). Compounds 1-5 inhibited Ab40 aggregation in a dosedependent manner. Moreover, compounds 2-5 protected SH-SY5Y cells from Ab toxicity. Therefore, these compounds are potential agents in AD treatment.Dementia is a neurodegenerative disease caused by acquired organic brain damage. The disease is characterized by a persistent loss of cognitive function that interferes with daily and social life. Alzheimer's disease (AD) is the most frequent cause of dementia 1 ; its pathological features include neuronal loss (mainly in the cerebral cortex), neurofibrillary tangles, and the occurrence of senile plaques in the brain parenchyma.Senile plaques are composed of amyloid-b (Ab) peptides. 2 Normally, Ab peptides are degraded and/or eliminated. However, excessive accumulation of Ab forms senile plaques, eventually leading to AD, which is known as the amyloid cascade hypothesis. 3 Ab is a partial fragment of amyloid precursor protein (APP), which is produced by the cleavage of b-secretase 1 (BACE1) and γ-secretase and is subsequently secreted into the extracellular milieu. [4][5][6] Ab undergoes degradation by various extracellular pathways. Therefore, 2025
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