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Increasing research indicates that AD\u00a0is a systemic disease, with a strong connection to cardiovascular disease. They share common genetic factors, such as mutations in the presenilin (PS1 and PS2) and the apolipoprotein E (APOE) genes. Cardiovascular conditions can lead to reduced cerebral blood flow and increased oxidative stress. These factors contribute to the accumulation of A\u03b2 plaques and the formation of abnormal tau protein tangles, which are both key pathological features of AD. Additionally, A\u03b2 deposits and abnormal protein responses have been observed in cardiomyocytes as well as in peripheral tissues. The toxic A\u03b2 deposition intensifies damage to the microvascular structure associated with blood\u2013brain barrier disruption and the initiation of neuroinflammation, which may accelerate the onset of neurocognitive deficits and cardiovascular dysfunction. 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