Retinoids are Vitamin A derivatives involved in cellular regulatory processes including cell differentiation, neurite outgrowth and defense against oxidative stress. Retinoids may also influence Amyloid beta processing upregulation of alpha secretase via ADAM10. Vitamin A and other retinoids also directly inhibit formation of Amyloid fibrils in vivo. These properties of retinoids are relevant to theories of Alzheimer's disease pathogenesis. Retinoids are already used in treatment of acne vulgaris, psoriasis, neuroblastoma and acute promyelocytic leukemia. Clinical studies involving in cognitively impaired older adults with Alzheimer's disease are beginning with a variety of retinoids. These studies need to address safety issues of retinoids in older populations, and hold hope for demonstrating efficacy in translating these basic mechanisms to treatment of a widespread dementing illness.

CVF defects were characterized by homonymous visual field defects or bilateral constriction. Eight of 9 patients progressed to probable or definite AD, but the CVF defects were distinctly different from those in typical AD. This observation probably reflects a posterior shift of cortical pathology to the primary and early secondary visual cortices in PCA. CVF testing should be considered in older patients with unexplained visual complaints, particularly when associated with difficulty driving, which may indicate the possibility of PCA and prompt early neurobehavioral evaluation.

Therefore, modulation of this type of cognitive flexibility does not seem to be mediated by the dopaminergic system. This suggests that the noradrenergic modulation of cognitive flexibility previously reported does not seem to extend to the dopaminergic system among catecholamines.

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