There is a large ongoing international effort to understand the pathogenic cascade underlying neurodegenerative diseases in order to rationally develop therapies. Here we investigate the role of two elements: 1) Changes in BKα channel expression, 2) Changes in lysosomal activity in crude synaptosomes from CSPα KO mice. CSPα is a presynaptic neuroprotective chaperone protein that, when mutated causes synaptic loss and neurodegeneration. BK channel KO, and intraperitoneal injections with chloroquine (lysosomal inhibitor), and Z-Phe-Ala-diazomethylketone which increases lysosomal activity did not halt neurodegeneration or alter the composition of crude synaptosomes. We report that a subset of endo-lysosomal proteins is present in crude synaptosomes.