Second, although we excluded subjects with a previous diagnosis of AS during year 2000 to increase the likelihood of identifying AS patients newly diagnosed in 2001, it was possible that some prevalent AS cases with more longstanding AS who had not sought medical care in 2000 but coded for the first time in 2001 based on our database, were included in the AS group. Third, due to the inherent limitation of the NHI database, information was lacking regarding lifestyle factors, such as Epimedoside-A smoking, alcohol consumption, and obesity. Moreover, since traditional vascular risk factors, such as diabetes, hypertension and dyslipidemia, are disorders with an insidious onset, some asymptomatic vascular risk factors may not be captured in the NHI database. Therefore, the prevalence of vascular risk factors may be underestimated in both the AS and non-AS groups. These Albaspidin-AA potential confounders may lead 
to residual confounding and may affect the interpretation of our findings. Fourth, the follow-up time was only 2 years and the long-term effects of AS on the development of ischemic stroke cannot therefore be evaluated. Finally, since Taiwanese are mainly of Chinese ethnicity, it is uncertain whether our findings can be generalized to other ethnic groups. In conclusion, the present population-based longitudinal followup study demonstrates there is an increased risk of ischemic stroke in young patients with AS and highlights the importance of early risk assessment for ischemic stroke in such patients. Further longterm follow-up study would be required to validate our findings and to investigate the underlying pathophysiological mechanism. Protein glycosylation regulates a wide range of processes critical to development and functioning of the central nervous system, including cell adhesion, cellular migration and differentiation, as well as synaptogenesis, synaptic efficacy and plasticity. The importance of glycosylation in the brain is underscored by the detrimental effects of impaired synthesis of glycoconjugates found in glycosylation congenital disorders, including developmental delays, progressive atrophy, psychomotor deficits, seizures, and strokes or stroke-like symptoms. The majority of brain glycoproteins are predicted to be N-glycosylated. In addition, proteins of the mammalian brain have the highest number of predicted N-glycosylation sites and the highest number of tissue specific N-glycosylated proteins, suggesting that brain-specific N-glycoproteins coevolved synergistically with its increasing anatomical and functional complexity. The ability to adapt and respond to environmental cues coevolved with the complexity of the mammalian brain, and depends on balanced excitatory synaptic transmission. Glutamate is the major neurotransmi er involved in fast excitatory transmission, which is primarily mediated by the AMPA subtype of glutamate receptor. AMPA receptors are responsible for postsynaptic depolarization, conveying fast ��point-to-point�� signaling of neurons. The AMPA receptor subunits are N-glycosylated after their biosynthesis in the lumen of the endoplasmic reticulum, yet the functional role of this pos ranslational modification is not well understood. Nglycosylation has no intrinsic effects on ligand binding or ion receptor conductivity.