New peptide strategy may protect brain cells involved in Parkinson's disease

Researchers at the Federal University of São Paulo (UNIFESP) have identified a potential new strategy for combating Parkinson’s disease using a peptide called Ac2-26, a fragment of the naturally occurring protein Annexin A1. Published in *Neuropharmacology*, the study—funded by FAPESP—showed that Ac2-26 reduced neuroinflammation and neuronal degeneration in mice models of the disease, which is characterized by the loss of dopamine-producing neurons. Parkinson’s disease currently lacks a cure, with treatments focusing on managing motor symptoms through levodopa, a dopamine precursor. However, long-term levodopa use can lead to reduced effectiveness and motor complications, prompting the need for alternative approaches. The peptide targets neuroinflammation, which affects both neurons and surrounding cells, potentially offering broader protection against brain cell death. In experiments, researchers induced Parkinson’s-like symptoms in mice by injecting a neurotoxic drug into their brains, then administered Ac2-26 intraperitoneally. The peptide demonstrated protective effects, particularly in male mice, where neuron loss was more pronounced. Female mice showed initial resilience to symptoms, but this advantage diminished over time regardless of Annexin A1 presence. The study also compared results in animals with and without the Annexin A1 protein, confirming the peptide’s anti-inflammatory properties. While Ac2-26 has been tested for other conditions, it has not yet been developed into a medication. Researchers emphasize that the findings are preliminary but suggest a promising new direction for Parkinson’s treatment beyond dopamine replacement. Cristiane Damas Gil, head of the Department of Morphology and Genetics at UNIFESP, noted that the peptide’s ability to mitigate inflammation could protect the brain more effectively than current therapies. Luiz Philipe de Souza Ferreira, a FAPESP scholar involved in the research, highlighted the need for alternative treatments due to levodopa’s limitations in long-term use.