The assays have also been compared with established Alzheimer’s disease biomarkers (CSF Aβ1–42 and Aβ-PET) and in relation to cognitive performance and cognitive decline (both baseline and longitudinal changes). The ratio of plasma Aβ1–42 to Aβ1–40 (denoted as Aβ42/40) identified abnormal amyloid CSF or PET status in individuals across the clinical Alzheimer’s disease continuum. In line with CSF or PET amyloid data, low plasma Aβ42/40 or the presence of misfolded Aβ1–42 are associated with cognitive decline and risk of progression to Alzheimer’s disease among cognitively unimpaired individuals, people with subjective cognitive decline, or individuals with mild cognitive impairment.  playing a key role in AD pathogenesis, have become a promising candidate for AD diagnosis. Furthermore, neuronal damage begins to occur 10–20 years before presenting the symptoms in AD patients, and amyloid plaques are late-stage pathological indicators of the disease.