Although the loss of vascular CLN-5 has typically been reported in brain pathologies (Biron et al., 2011), previous studies have also shown that it can be redistributed and support peripheral leucocyte infiltration during neuroinflammation (Paul et al., 2016; Stankovic et al., 2016) and that CLN-5-positive extracellular vesicles potentially increase near the surface of brain vessels in human AD (Villar-Vesga et al., 2020). This evidence concerns the gene CLN5 and Alzheimer disease.