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. 2020 Jun 23;22(8):72. doi: 10.1007/s11886-020-01318-w

Table 1.

Summary of the key findings reported in this review

Disease determinant Notable feature Key findings Ref
Reduced cerebral perfusion Oxidative stress • Hypoxia-induced cellular respiration exhaustion and increased ROS production, promoting cell, and BBB injury [2123]
• Worsened by Aβ build-up and consequent mitochondrial dysfunction [2426]
Aβ accumulation • Reduced Aβ clearance via BBB, interstitial bulk flow, and/or meningeal lymphatic impairment [27, 28]
• Reduced Aβ clearance via BBB, interstitial bulk flow, and/or meningeal lymphatic impairment [2933]
Inflammation • Reduced microglial presence and functioning around Aβ plaques, impairing Aβ internalization and clearance [34]
Cardiovascular changes Diastolic dysfunction • Preserved EF accompanied by high filling pressures, weakened myocardial contractility, reduced peripheral vasodilation, diminished HR response, and less organ perfusion [3548]
• Retrospectively, HFpEF and LV hypertrophy were more likely to be seen in AD patients [6]
Arterial stiffness, increased central pulsatility • Associated with decreased peripheral BF, central Aβ accumulation, BBB injury, cerebrovascular compromise, and brain hypoperfusion [4951]
Genetic variants Presenilin (PSEN) -1 and − 2 • Same variants associated with both early-onset AD and sporadic iDCM [4]
• Promoter-specific variants have been observed in iDCM but not yet AD [4]
Protein aggregation Brain deposition • AD aggregates composed of Aβ, tau, metal ions, and chaperones [52]
• Cofilin rods implicated in AD neuritis [53]
Heart deposition • Aggregates have been identified in atrial fibrillation, cardiac amyloidosis, and cardiomyopathies—notably, cofilin was isolated from iDCM aggregates [4, 6, 54]
• Aβ and PAO deposits seen in AD patients [7•]
Systemic alterations Peripheral Aβ accumulation • Aβ peripheral clearance impaired by decreased scavenger receptors, less proteolytic enzymes, and liver/kidney malfunctioning [5558]
• BBB damage promotes Aβ release into the periphery and potential seeding to other organs [27, 59]
Peripheral Aβ Production • Promotes central Aβ deposition and associated inflammation [6064]
Exosome trafficking • Help carry Aβ locally and systemically following Aβ endocytosis or APP cleavage [6567]
• Bring MiR-1 from ischemic myocardium to hippocampus, inducing microtubule damage [68•]