SK-129 aims to prevent formation of toxic protein clumps

Written by Patricia Inácio, PhD | April 8, 2026

• Parkinson's and related diseases involve toxic alpha-synuclein protein clumps.
• SK-129, a lab-made molecule, reduced these toxic protein clumps and their spread.
• It crossed the blood-brain barrier, showing promise for slowing disease progression.

A small, lab-made molecule called SK-129 reduced the formation of toxic clumps of the alpha-synuclein protein, a hallmark of Parkinson’s disease, a study found.

SK-129 was able to cross the blood-brain barrier – a semipermeable membrane that protects the brain and central nervous system – and prevent damage caused by these toxic clumps, as well as their spread across the brain.

The findings may also be relevant to other Parkinson’s-like diseases characterized by abnormal clumping of the protein alpha-synuclein, including Lewy body dementia and multiple system atrophy.

“This is an important step toward developing treatments that target the root cause of these diseases,” Mazin Magzoub, PhD, associate professor of biology at NYU Abu Dhabi and a co-lead author on the study, said in a New York University press release. “Instead of only treating symptoms, we are working toward slowing or stopping the disease itself.”

The study, “Foldamers rescue synucleinopathy phenotypes in multiple in vitro and in vivo models,” was published in the journal Science Translational Medicine.

Misfolded protein forms toxic clusters

Parkinson’s disease is caused by the progressive loss of dopamine-producing neurons, a type of nerve cell important for movement control.

A hallmark of Parkinson’s and related disorders, collectively known as synucleinopathies, is the formation of toxic clumps of the protein alpha-synuclein in brain cells. In healthy neurons, alpha-synuclein normally exists in a monomeric (single-molecule) form and is involved in nerve cell communication.

But when the protein misfolds, it can assemble into small toxic clusters called oligomers, which then form larger aggregates that make up Lewy bodies, a key disease-causing feature of Parkinson’s. These clumps contribute to cell death and spread in a prion-like manner, meaning aggregates in one brain region may trigger more misfolding in nearby regions.

That means preventing alpha-synuclein from clumping and spreading is seen as a promising strategy for treating synucleinopathies.

Researchers at NYU Abu Dhabi and the University of Denver focused on the potential of foldamers, lab-made molecules designed to mimic features of natural proteins. Specifically, they investigated SK-129, a foldamer designed to inhibit alpha-synuclein aggregation.

In lab tests, they found that SK-129 blocked alpha-synuclein from clumping together and reduced disease-related effects across several lab models, including nerve cells derived from human induced pluripotent stem cells (iPSCs) and animal models such as the worm Caenorhabditis elegans and mice. iPSCs are cells that can generate almost any type of cell in the body.

How our last dog watched over my husband after his diagnosis

Written by Jamie Askari | Feb. 18, 2025

Growing up, we always had a dog in our family. My mom was particularly fond of schnauzer breeds, so I always had a gray-haired, old-man-looking dog to walk, feed, and keep me company. One dog, Charlie Brown, came into our family a few years before I was born, so we grew up together. After he passed over the rainbow bridge to doggy heaven, I was devastated, as I’d never known life without dear Charlie.

Fast forward to my life as a mom of three young children. My daughters had been begging and pleading for a pet for years, and the closest they’d gotten was when I announced I was pregnant with their brother. While they were excited about baby Jake, they continued in their pursuit of a pet.

By the time Jake was 2 years old, my husband, Arman, and I finally relented. We found a darling Cavalier King Charles spaniel and poodle mix that was being sold by a breeder only a few hours away. Not only was he the runt of the litter, but he was the only dog left that hadn’t been adopted. Although Arman also grew up with dogs, he’s not an animal lover by any means. When he saw the picture of the dog online, he simply said, “That’s our dog.”

When the time came to pick up our puppy, we piled into our large SUV and drove three hours to a farm in southwestern Ohio. As soon as the dog saw us, he jumped into our car and never looked back at that farm; he somehow knew that we were his family now. The girls named him Duke, after a character in a movie they loved. We referred to Duke as a small dog with a big name.

Duke was with our family as our kids became school-age, teenagers, and eventually young adults. He was beside me as we watched the school bus pull away every morning. He stood patiently by the door while I waited for the kids to return home by bus in the afternoon. He was just as excited as I was to hear about their day, and, of course, he loved the crumbs and scraps from their snacks.

Enter Parkinson’s

After Arman was diagnosed with early-onset Parkinson’s disease in 2009, Duke seemed to look at him differently. I’m convinced that he knew Arman was struggling with something, but he wasn’t sure exactly what. He would stare at Arman, his eyes blue and glassy with cataracts at the end, and you could just tell that Duke was feeling my husband’s pain.

New research lays groundwork for safer, more tailored deep brain stimulation

Written by Marisa Wexler, MS | April 6, 2026

• The findings from new research in China may enable personalized deep brain stimulation for people with Parkinson's.
• The study's scientists used MRI scans to track brain circuit changes during DBS treatment.
• The researchers say this work allows them to better understand how this type of Parkinson's treatment influences brain biology.

Scientists have demonstrated that it is possible to collect individualized data on how connections among brain circuits change for people with Parkinson’s disease who are undergoing deep brain stimulation (DBS) as a treatment for their symptoms.

These findings lay the groundwork for more individualized approaches for DBS, and also provide a new resource for researchers to better understand how this type of Parkinson’s treatment influences brain biology, according to the team.

The data were described in “Circuit response to neuromodulation characterized with simultaneous deep brain stimulation and precision neuroimaging in humans,” a study published in the journal Nature Neuroscience. The work was funded mainly by the National Key Research and Development Program of China and the National Natural Science Foundation of China.

The senior author of the study, Hesheng Liu, PhD, is the cofounder and chief scientific officer of Galaxy Brain Scientific, a China-based company that is working to advance personalized DBS approaches for Parkinson’s and other neurological disorders.

“Our goal is to redefine the treatment paradigm for brain disorders,” Liu said in a company press release detailing the findings. According to Galaxy, “this study establishes the world’s largest longitudinal … dataset to date” on DBS and MRI brain imaging scans.

“By moving from ‘one-size-fits-all’ to ‘one-person-one-strategy,’ we are now pioneering the application of this technology to treat complex conditions beyond Parkinson’s, including autism and Alzheimer’s disease,” Liu said.

Parkinson’s is a neurological disorder in which certain brain cells sicken and die, leading to disruptions in brain signaling that ultimately give rise to disease symptoms.

DBS is a surgical treatment for Parkinson’s in which tiny electrodes are implanted into the brain to deliver gentle electrical stimulation to specific brain regions. DBS is well-established as an effective approach for managing certain Parkinson’s symptoms.

Nonetheless, there’s often a lot of trial and error involved in finding the exact right settings to ease symptoms for each individual.

Each person decides when to share, who to tell, and how much to say

Written by Crystal Onyema | April 1, 2026

One of the initial things I didn’t understand when I became a Parkinson’s caregiver was that not everyone is ready to share their diagnosis right away. From the outside, it can feel like something that should just be said so that people understand what’s going on. But for my late uncle Brandon, it wasn’t that simple. What he was dealing with was real, but how and when he chose to share it was his own decision.

I saw this most clearly when he was with his friends, people who had known him for decades. They understood his sense of humor and how easily he could keep a conversation going. That was just him. So when he started speaking more slowly or took longer to answer, it didn’t seem like anything was different at first.

One of his closest friends laughed about it once, thinking he was just joking like usual and trying to make the moment last. I could see why they thought that. They were responding to the person they had always known. But they didn’t know he was living with Parkinson’s disease. He wasn’t ready to share that yet, and in that moment, I felt like I was carrying a quiet truth that no one else was in on.

Everyone has their own timing

Even early on, I could see that he knew things were changing. He still acted like himself, kept things light, and used humor to try to stay in a conversation. But there were small pauses that felt different. Sometimes I noticed him working harder to find his words or to keep up, even if no one else saw it. It wasn’t denial or avoidance. It was about timing and attempting to maintain control in a situation where so much felt uncertain.