Targeting α-Synuclein with Antisense Oligonucleotides to Slow Parkinson’s Disease
Parkinson’s disease is driven by the spread of misfolded α-synuclein through the nervous system and brain. Misfolded α-synuclein can cause harmful aggregates and damage neurons as it moves between cells, leading to disease symptoms. Suppressing the expression of α-synuclein can slow the progression of the altered form, offering a potential treatment option for Parkinson’s disease. Using antisense oligonucleotides (ASOs) to target α-synuclein expression has shown promise in controlling the disease’s progression.
ASOs are engineered compounds that can degrade target mRNA, leading to reduced levels of the corresponding protein. They offer a unique advantage over other approaches by specifically controlling intracellular levels of normal α-synuclein, potentially providing a safer and more effective treatment option. Researchers have tested the localized administration of ASOs in mouse brains, observing a significant decrease in Lewy body-like pathologies and a potential prevention of abnormal fibril-induced aggregate spread.
For more information, visit the link: https://www.tmd.ac.jp/english/press-release/20240607-1/
