In dogs with CCD, plasma Aβ42, a longer Aβ isoform which is more fibrillogenic and associated with disease, was monitored as a biomarker potentially linked to CCD (González-Martínez et al., 2011; Schütt et al., 2015). One study showed highest Aβ42 plasma levels in younger healthy dogs, and significantly higher Aβ42 plasma levels in mildly cognitively impaired dogs in comparison to severely impaired dogs (González-Martínez et al., 2011). However, another study reported the opposite with highest Aβ42 plasma levels in CCD dogs (Schütt et al., 2015). Plasma ratio of Aβ40 and Aβ42, was shown to be similar in human AD and CCD as in healthy individuals (Mayeux et al., 2003; Lopez et al., 2008; González-Martínez et al., 2011) although in some studies decreases in plasma Aβ42 were an indicator of faster progression of CCD and AD (Pesini et al., 2009; González-Martínez et al., 2011). This points to a possible disease mechanism wherein aggregation and accumulation of Aβ in the brain results in lower levels of Aβ in plasma and CSF. A more recent human study showed decrease in plasma Aβ during the dementia stage of AD and increased levels of Aβ in plasma during vascular disease (Janelidze et al., 2016).