CD200 is expressed in neurons and oligodendrocytes, astroglia and endothelial cells, while CD200R is expressed in microglia. CD200 and its receptor are decreased in regions with severe AD pathology. In reference to the neurotrophic factors PEDF and BDNF, and the structural GFAP, our experiments revealed very little agerelated fluctuation for PEDF and BDNF, although GFAP significantly increased between YA and OO age groups in the PCG. Other investigators have also shown that the presence of GFAP increases with age. Intriguingly, S100B demonstrated a large and statistically significant difference among the studied groups which was more evident between the YA and OO, being substantially elevated in the Bumetanide latter group. S100B is a multifunctional protein that, like GFAP, is relatively restricted to astrocytes and has served as a marker for brain damage in neurodegenerative diseases. This molecule has a deleterious role in hypoxia/ischemia and stroke where it increases gliosis, infarct expansion and proinflammatory activity. Ironically, S100B also has a powerful neuroprotective function on cholinergic neurons of the nucleus basalis of Meynert during oxygen and glucose deprivation. We quantified key molecules in the Pc and PCG brain regions which exhibit early pathological alterations in AD. In general, the Sulfamerazine majority of molecules assessed showed decreased levels in the OO group relative to YA and MA cases or remained unchanged in a few instances. Interestingly, S100B, a molecule with neuroprotective activity, exhibited substantial increases with advancing age in both PC and PCG. A salient observation was that even in two closely adjacent areas of the cerebral cortex, like the Pc and PCG, the levels of some molecules substantially differ which may be explained by anatomical and functional heterogeneity. The kinetics and role of Ab accumulation in the pathogenesis of AD still presents a major conundrum in understanding the clinical progress of dementia. Our results indicate that some non-demented nonagenarian individuals free of parenchymal and vascular amyloid deposits did not develop AD pathology to the same degree as that observed in demented AD subjects.