FIGURE 1.

Variable mechanisms by which AD patients with non-genetic risk factors manifest cognitive dysfunction. The mechanisms whereby non-genetic risk factors modify cognitive dysfunction are divided into four elements: short- and long-term effects of vascular and metabolic factors. These are (1) compromised vascular reactivity, (2) vascular lesions, (3) hypo/hyperglycemia, and (4) exacerbated AD histopathological features, respectively. AD histopathological features include β-amyloidosis and pathological tau. β-amyloid also compromises vascular reactivity and causes microhemorrhages due to cerebral amyloid angiopathy. The contribution of these four elements to manifestation of cognitive dysfunction varies among patients, though all components must not always be present.