Factors implicated in Alzheimer’s disease

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Several factors have been implicated in Alzheimer’s disease (AD) but there is no definite conclusion as to the main pathogenic agents. Mutations in the amyloid precursor protein (APP) that lead to increased production of amyloid beta (Abeta) peptide are associated with the early onset, familial forms of AD. However, in addition to aging, the most common risk factors for the sporadic, prevalent form of AD are hypertension, hypercholesterolemia, ischemic stroke, the ApoE4 allele and diabetes, all characterized by a vascular pathology. In AD, the latter includes accumulation of Abeta in the vessel wall, vascular fibrosis, and other ultrastructural changes in constituent endothelial and smooth muscle cells. Moreover, the ensuing chronic cerebral hypoperfusion has been proposed as a determinant factor in the accompanying cognitive deficits. In transgenic mice that overexpress mutated forms of the human APP (APP mice), the increased production of Abeta results in vascular oxidative stress and loss of vasodilatory function. The culprit molecule, superoxide (.O2(-)), triggers the synthesis of other reactive oxygen species (ROS) and the sequestration of nitric oxide (NO), thus impairing resting cerebrovascular tone and NO-dependent dilations. The Abeta-induced cerebrovascular dysfunction can be completely abrogated in aged APP mice with antioxidant therapy. In contrast, in mice that overproduce an active form of the cytokine transforming growth factor-beta1 (TGF-beta1, TGF mice) and recapitulate the vascular structural changes seen in AD, antioxidants have no beneficial effect on the accompanying cerebrovascular deficits. The present review discusses the beneficial role and limitations of antioxidant therapy in AD cerebrovascular pathology. By PubMed - as supplied by publisher

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