Issue link: https://cp.revolio.com/i/1219209
Page 30 | Abby's Magazine - www.AbbysMag.com An Osaka University-led research team has recently published findings that provide a ray of hope for the millions of Parkinson's disease (PD) sufferers worldwide. Although more common in those aged over sixty, PD can strike at any age, with an es mated prevalence of 41 per 100,000 people in their for es. And while not fatal in and of itself, the progressive neurodegenera on that is characteris c of PD can o en cause secondary effects that lead to death. The exact cause of PD is s ll a mystery, but researchers believe that both gene cs and the environment are likely to play a part. Importantly though, all PD pa ents show a loss of dopaminergic neurons in the brain and increased levels of a protein called α-synuclein, which accumulates in Lewy bodies. Lewy bodies are a pathological feature of both familial and sporadic forms of the disease, as well as some types of demen a. In the study published in Scien fic Reports, the team led by researchers from Osaka University's Graduate School of Medicine focused on α-synuclein as a target for a novel PD treatment. "Although there are drugs that treat the symptoms associated with PD, there is no fundamental treatment to control the onset and progression of the disease," explains lead author Takuya Uehara. "Therefore, we looked at ways to prevent the expression of α-synuclein and effec vely eliminate the physiological cause of PD." To do this, the researchers designed short fragments of DNA that are mirror images of sec ons of the α-synuclein gene product. The constructs were stabilized by the addi on of amido-bridging. The resul ng fragments, called amido-bridged nucleic acid-modified an sense oligonucleo des (ASOs), bind to their matching mRNA sequence, preven ng it from being translated into protein. PArkinSon'S DiSeASe Before it Starts A er screening 50 different ASOs, the researchers se led on a 15-nucleo de sequence that decreased α-synuclein mRNA levels by 81%. "When we tested the ASO in a mouse model of PD, we found that it was delivered to the brain without the need for chemical carriers," says co- lead author Chi-Jing Choong. "Further tes ng showed that the ASO effec vely decreased α-synuclein produc on in the mice and significantly reduced the severity of disease symptoms within 27 days of administra on." Explains senior author of the study Hideki Mochizuki, "Our results showed that gene therapy using α-synuclein-targe ng ASOs is a promising strategy for the control and preven on of PD. We expect that in the future, this method will be used to not only successfully treat PD, but also demen a caused by α-synuclein accumula on." By Osaka University STo PP i n G