Data from: Selective loss of primary cilia and neurotrophic signaling in G51D α-synuclein mice highlights a common pathway to Parkinson’s disease

Parkinson’s disease is characterized by dopaminergic neuron loss and
accumulation of α‑synuclein aggregates in the brain. G51D α‑synuclein
knock‑in mice provide a genetically and clinically relevant model of
disease, exhibiting early olfactory deficits, age‑dependent motor
impairment, and progressive phospho‑α‑synuclein accumulation. In multiple
Parkinson’s disease models, striatal cholinergic and parvalbumin
interneurons, as well as astrocytes, lose primary cilia and the
neurotrophic signaling needed to sustain dopaminergic neurons. We show
here that G51D-α‑synuclein mice share these phenotypes. Phospho‑Ser129
α‑synuclein accumulation correlates with cilia loss in cholinergic
interneurons but not in medium spiny neurons that accumulate higher
phospho‑α‑synuclein levels. In the piriform cortex, parvalbumin neurons
lose primary cilia and downregulate Neurturin, potentially contributing to
olfactory dysfunction. Within the peripheral olfactory epithelium,
horizontal basal cells lose cilia, whereas multi-ciliated olfactory
sensory neuron cilia remain intact. These findings reveal convergent
cellular vulnerabilities across Parkinson’s disease models and highlight a
pathogenic role for impaired ciliary signaling.