Abstract

The occurrence of chronic and neurodegenerative diseases is epidemiologically important in elderly population, including Alzheimer’s Disease (AD). Risk factors such as diabetes, obesity, hypertension, Cardiovascular Diseases (CVD), hyperlipidemia, hyperhomocysteinemia, and smoking can lead to Cerebrovascular Diseases (CBVD). The neurodegeneration is consequence of cumulative macro and microcirculatory damage, corroborating to increase in systolic pressure, neuroinflammation, oxidative stress, and excitotoxicity. There are some intersections between AD and CVD. For example, e4 allele of the Apolipoprotein E (APOE) gene is a risk; low plasma levels of ApoE protein favor the risk of AD, regardless of the APOE genotype. Furthermore, the insulin resistance causes atrophy of the white matter with loss of myelinated fibrils. These phenomena modify the function of the Blood-Brain Barrier (BBB), causing injury to pericytes and activation of the Cell Adhesion Molecule-1 (VCAM-1), Intercellular Adhesion Molecule-1 (ICAM-1) and E-selectin. In consequence, it is observed excitotoxicity, predisposing to ischemic stroke, activation of neuroinflammation, excessive production of Beta-Amyloid Protein (Aβ42) and aberrantly phosphorylated tau, activation of astrocytes evidenced by overexpression of Glial Fibrillar Acid Protein (GFAP), inhibition of neurotransmitter uptake, excessive depolarization of neurons efferent and decrease on expression of Brain-Derived Neurotrophic Factor (BDNF). Thus, future experimental and population-based studies are encouraged.

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