SPG11 encodes spatacsin, a 280 kDa protein that plays a critical role in vesicle trafficking and autophagy-lysosomal machinery function 1. The protein is essential for maintaining neuronal integrity, particularly affecting the corticospinal tracts and other neuronal populations. SPG11 mutations cause the most frequent form of complex autosomal recessive hereditary spastic paraplegia (SPG11-HSP), representing a significant proportion of hereditary spastic paraplegia cases 2 3. The disorder typically manifests with progressive lower limb weakness and spasticity, but exhibits a heterogeneous phenotype that can include cognitive decline, thin corpus callosum, peripheral neuropathy, and various movement disorders such as dystonia, tremor, and parkinsonism 1 4. SPG11-HSP represents a unique example of a disorder bridging neurodevelopmental and neurodegenerative processes, with spatacsin dysfunction affecting both neuronal development and maintenance 1 5. The protein's involvement in autophagy dysfunction places it within an emerging group of genetic diseases affecting core autophagy machinery components, which share recognizable clinical signatures including neurological, neuromuscular, and multisystem manifestations 5. Disease onset and progression can vary significantly, even among patients with identical mutations 6.