Trilink社 Research Update: Splicing to Save Memory
Alzheimer’s Disease (AD) is the most common form of dementia or progressive memory loss, affecting 5.8 million Americans. Approximately 90% of AD patients have the late-onset form of the disease, which presents with symptoms in the patient’s 60s. Late-onset AD is caused by a combination of environmental, lifestyle, and genetic risk factors, including single nucleotide polymorphisms (SNPs). However, a better understanding of the biological impact of these SNPs and how they could be treated remains a work in progress.
A SNP in exon 2 of the CD33 gene has been shown to reduce susceptibility for late-onset AD. This CD33 SNP affects alternative splicing in the CD33 mRNA. In the brain, CD33 is expressed primarily in microglial cells. Microglial activation is thought to prevent proper innate immune degradation of the beta amyloid plaques that accumulate to cause AD. The presence of this SNP leads to exon 2 exclusion, in turn reducing CD33 expression and, potentially, microglial activation. However, little is known about CD33 exon 2 splicing regulation...
Two New Co-transcriptional mRNA Capping Patents
TriLink BioTechnologies announced today that the United States Patent and Trademark Office has issued two new patents to the company. Both patents cover advancements in TriLink’s CleanCap® technology for the co-transcriptional capping of messenger RNAs (mRNAs).
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