Researchers at the Federal University of São Paulo (UNIFESP) in Brazil announced on June 12 that they have identified a new approach that may help protect neurons and other brain cells involved in Parkinson's disease. The findings, based on experiments conducted in mice, were published in the journal Neuropharmacology.
The research team evaluated the effects of a peptide called Ac2-26, which is a fragment of the protein Annexin A1. This protein occurs naturally in both rodents and humans. Previous animal studies have shown that Annexin A1 can control neuroinflammation linked to Parkinson's disease and reduce neuronal degeneration.
Parkinson's disease primarily affects neurons responsible for synthesizing and releasing dopamine, an essential neurotransmitter for motor functions, motivation, reward, and pleasure. As these neurons degenerate due to the disease, patients lose the ability to synthesize dopamine, resulting in symptoms such as freezing of gait and tremors.
"It's still an experimental study in its very early stages, but it offers an interesting approach by presenting a different strategy from conventional treatment. The peptide acts on neuroinflammation rather than on dopamine replacement. That's important because, in neurodegenerative diseases, there's an inflammatory reaction that affects not only neurons, but also surrounding cells, and the peptide mitigates that process, consequently protecting the brain from cell death," said Cristiane Damas Gil, head of the Department of Morphology and Genetics at the São Paulo School of Medicine (EPM) at UNIFESP and author of the study.
Currently there is no cure for Parkinson's disease; treatments focus mainly on controlling motor symptoms caused by dopamine deficiency through medications like levodopa. "This medication is considered the gold standard, offering significant benefits especially in the early stages or during acute treatment when it leads to a marked improvement in motor symptoms. However, long-term use diminishes its effectiveness and can lead to development of motor complications and fluctuations in therapeutic response. That's why it's essential to seek treatment alternatives for such a complex disease as Parkinson's," said Luiz Philipe de Souza Ferreira, who conducted this research as part of his FAPESP scholarship.
The researchers simulated Parkinson’s disease by injecting a neurotoxic drug into mice brains while administering Ac2-26 intraperitoneally almost simultaneously. They observed differences between male and female mice: females initially performed better on movement tests after injury simulating Parkinson’s but this difference faded over time even without Annexin A1 protein present; males showed more evident neuron loss allowing clearer assessment of Ac2-26’s protective effects against degeneration. The experiments also indicated changes to reproductive cycles among female mice with induced Parkinson’s symptoms—highlighting impacts on their endocrine system—and suggested future protocols should consider biological sex differences.
Gil concluded, "Our next step is to investigate whether the peptide can reverse damage caused by Parkinson's disease. If that's proven then the peptide becomes a more promising treatment candidate."
