Neurodegeneration begins inside the cell. Deep inside.

Over 11 million people live with Parkinson’s disease today, and nearly 57 million with Alzheimer’s and related dementias. These numbers will grow. Disease-modifying treatments remain out of reach for most patients.
The reason, increasingly, points to where we have been looking.

𝗪𝗵𝘆 𝗹𝘆𝘀𝗼𝘀𝗼𝗺𝗲𝘀?
Neurons are post-mitotic and extraordinarily long-lived. They cannot dilute accumulated damage through division. Their survival depends on a continuous, high-fidelity degradation system, and that system ends in the lysosome.
Genes regulating lysosomal function are now directly implicated in Alzheimer’s, Parkinson’s, and ALS. Lysosomal acidification defects, impaired autophagy, and defective protein degradation are core pathological mechanisms, not downstream consequences. When the lysosome fails, alpha-synuclein aggregates accumulate, amyloid-beta escapes clearance, and neuronal death follows.

𝗔 𝗻𝗲𝘄 𝗰𝗹𝗮𝘀𝘀 𝗼𝗳 𝘁𝗮𝗿𝗴𝗲𝘁𝘀 𝗶𝘀 𝗲𝗺𝗲𝗿𝗴𝗶𝗻𝗴
Among the most compelling lysosomal ion channel targets in neurodegeneration:

✔️ 𝐓𝐌𝐄𝐌𝟏𝟕𝟓 – a lysosomal K⁺/H⁺ channel that stabilises luminal pH and regulates GCase activity. Its loss-of-function variant is the top hit at a major Parkinson’s GWAS locus, with first-in-class selective inhibitors identified in 2024.

✔️ 𝐓𝐑𝐏𝐌𝐋𝟏 – the lysosomal calcium release channel, with established roles in autophagy flux, lysosomal exocytosis, and membrane repair across Parkinson’s and lysosomal storage diseases.

Both targets share a critical constraint: they can only be studied meaningfully in native lysosomal membranes. And reaching the level of quality and physiological relevance that Drug Discovery requires is why we developed 𝐋𝐘𝐒𝐎-𝐏𝐫𝐞𝐩™.