However, the presence of APOE e4 is not a deterministic factor for AD because many carriers will never develop this condition during their lifetimes. Intriguingly, ApoE in AD is abundantly present in both cerebrovascular and parenchymal amyloid deposits. Apolipoprotein E must therefore play an important function in the vascular and parenchymal deposition of Ab and possibly function as an in situ catalytic effector in Ab polymerization. Moreover, ApoE may also participate in the association of Ab with molecules of the extracellular matrix which are abundant in the amyloid deposits. Our MA and OO PF-5274857 groups were specifically selected on the basis of not being demented and having no or very low amyloid plaque scores. Hence, it was interesting to Chlorhexidine hydrochloride observe that the allelic frequency of APOE e4 was reduced to one heterozygous individual among the 11 MA and OO participants in the study. There were no observable differences in the levels of ApoE among the 3 age groups, as determined by ELISA. Western blots of ApoJ demonstrated 2 bands that corresponded to ApoJ-a and ApoJ-b chains with a more abundant representation of the former. The functional dimeric ApoJ is also capable of binding and transporting Ab peptides. In both the Pc and PCG, there was a noticeable increase of both isoforms in the MA group relative to the YA and a subsequent decrease in OO subjects which may be associated to age-related atrophy. On the other hand, recent studies have demonstrated that in non-demented individuals elevated CSF ApoJ correlates with a substantial degree of entorhinal cortex atrophy assessed by MRI, apparently independent from elevated p-tau, suggesting that ApoJ may hasten the progression of neurodegeneration. Mild but chronic inflammation has been observed in senescent cells and the aging brain and neuroinflammation is common in neurodegenerative diseases. In the absence of neurodegeneration and Ab deposition, there were no significant changes in the levels of TNF-a among the 3 groups under study.On the other hand, levels of CD200 decreased with age in the PCG. CD200 and its receptor CD200R are capable of generating anti-inflammatory signals that when deficient, as it occurs in disease or aging, may exacerbate chronic neuroinflammation.