Longitudinal studies have indicated that lower levels of Aβ42 in CSF can be detected as early as 18 years before the clinical manifestation of AD symptoms [11], alongside an elevated presence of AD-related proteins, such as apolipoprotein E (APOE), clusterin (CLU), Aβ precursor protein (APP), and complement component 7 (C7), all of which are implicated in Aβ clearance [12, 13], immunological surveillance, and protection [14]. Here, APP is linked to Alzheimer disease.