Authors: Nadia G. Innamorato, Agnieszka Jazwa, Ana I. Rojo, Concepción García, Javier Fernández-Ruiz, Anna Grochot–Przeczek, Anna Stachurska, Alicja Jozkowicz, Jozef Dulak, Antonio Cuadrado
DOI: 10.1371/journal.pone.0011838
Abstract Summary
Nrf2 activation shows promise for Parkinson’s therapy, but concerns existed about its target gene HO-1 potentially causing iron buildup and neurotoxicity. Using knockout mice and MPTP-induced Parkinsonism, researchers found Nrf2 deficiency worsened neurodegeneration, while HO-1 absence had no effect. Neither protein significantly influenced iron accumulation, suggesting HO-1 is neutral and Nrf2 activation could safely benefit Parkinson’s patients.
Why Brain? 🧠
Nrf2 activation protects against Parkinson’s toxin damage in mice, while its target HO-1 shows no effect, suggesting Nrf2 as a promising therapeutic target without iron-related toxicity concerns.
The image is AI-generated for illustrative purposes only. Courtesy of Midjourney.
