Table 1.
Mechanism hypothesis | References |
---|---|
Hemorrhagic and ischemic stroke induce Aβ deposits and CAA leading to dementia |
Ellis et al. [10] Regan et al. [3] Gamaldo et al. [11] Pendlebury and Rothwell [124] Savva et al. [123] Cordonnier and van der Flier [9] Cerasuolo et al. [122] |
Stroke induces Aβ accumulation within the cerebrovascular system by decreasing Aβ clearance | Garcia-Alloza et al. [121] |
Stroke-induced hypoxia leads to an overexpression of APP |
Rensink et al. [127] Ashok et al. [130] |
Stroke-induced BBB breakdown allows blood Aβ infiltration within the brain parenchyma |
Yang and Rosenberg [128] Hawkes et al. [49] Ramanathan et al. [53] |
Oxidated LRP-1 in AD or after stroke cannot interact properly with circulating Aβ |
Donahue et al. [63] Ramanathan et al. [53] Ashok et al. [130] Liu et al. [82] Zlokovic et al. [60] |
Post-stroke Aβ accumulation leads to inflammatory processes and neurodegeneration, typical in dementia |
Zlokovic [131] Kinnecom et al. [132] |
Lack of Aβ-RAGE complexes after stroke leads to a pro-inflammatory cascade and Aβ accumulation, which can contribute to neurotoxicity |
Deane et al. [61] Liu et al. [62] |
Correlation between Aβ deposits and sleep disorder is a common risk factor for stroke and AD |
Holth et al. [95] Ma et al. [96] Joa et al. [97] |
CSF clearance and the glymphatic system are impaired with both stroke and AD, leading to accumulation of waste metabolites in the brain |
Silverberg et al. [145] Weller et al. [16] Weller et al. [6] Kress et al. [14] Gaberel et al. [17] Peng et al. [15] Goulay et al. [18] Lundgaard et al. [90] Borwn et al. [19] |
CAA and AD are associated with modifications in perivascular spaces, which can lead to flow disturbance, stroke, and Aβ accumulation |
Mendelsohn and Larrick [92] Kress et al. [14] Hawkes et al. [49] Van Veluw et al. [100] Banerjee et al. [99] Charidimou et al. [118] |