English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance Degeneration of midbrain dopamine neurons is the main pathological hallmark of Parkinson’s disease. Identifying transcriptional programs that maintain these neurons in the adult brain will help us understand their specific vulnerability. Here, we show that the survival of dopaminergic neurons requires the ongoing action of LIM-homeodomain transcription factors Lmx1a and Lmx1b. We discovered an Lmx1a/b-dependent pathway maintaining mitochondrial functions in midbrain dopaminergic neurons. Accordingly, ablation ofLmx1a/b results in impaired respiratory chain activity, increased oxidative stress, and mitochondrial DNA damage and causes Lewy neurite-like pathology. Importantly, deletion ofLmx1a/b links metabolic impairment, α-synuclein inclusions, and progressive neuronal loss. Modulation of this pathway opens new strategies to slow down or prevent the death of vulnerable neurons in Parkinson’s disease.

Lmx1a and Lmx1b regulate mitochondrial functions and survival of adult midbrain dopaminergic neurons