Feature | Description | ASA’s effect |
---|---|---|
Ischemic stroke | MS patients may have an increased risk of stroke [17, 18, 20, 36, 37]. | ASA reduces the risk of ischemic stroke in some subjects, for example, those who had a previous stroke [24–26, 79]. ASA decreases platelet activation and aggregation through irreversible inhibition of platelet COX-1, and the resultant decrease in TXA2 production has a cardioprotective effect [57, 64]. It is unknown whether the risk of strokes in MS patients will be reduced in response to ASA. |
Thrombosis | MS patients have an increased risk of venous thrombosis [18, 19, 21–23, 39]. | ASA lowers the incidence of venous thrombosis in some subjects, for example, orthopedic surgery patients and those who experienced an unprovoked venous thromboembolism [27, 28, 88]. It is not known whether the risk of venous thrombosis is reduced in response to ASA in MS patients, but ASA reduces the risk for first thrombosis in patients with APLAs [107]. |
A higher percentage of MS patients have APLAs than controls [96–98]. APLAs are a diagnostic feature of APS, which involves thromboses. | ||
Platelets | Platelets are activated in MS and have been implicated in contributing to MS pathogenesis, such as by promoting inflammation [71, 72, 111]. | Anticoagulants decreased the severity of EAE [110, 211]. ASA lowers one indicator of platelet activation in MS patients. |
Fibrin | Limiting fibrin formation reduced EAE disease activity [114, 115]. Fibrin deposition may activate microglia [113]. | ASA may lessen fibrin deposition and induce fibrinolysis [116]. |
Thrombin | Is thought to promote inflammatory disease states of the CNS [117], and thrombin is associated with multiple pathological features in EAE [118]. | ASA may decrease thrombin at microvascular injury sites [119]. |
Microglia | Activated microglia can have a pro-pathogenic role in MS [3–5]. | ASA may reduce production of proinflammatory cytokines and reactive oxygen species (ROS) by microglia [155–157]. |
Inflammation | Multiple components of inflammation (for example, ROS, proinflammatory cytokines) are thought to contribute to MS pathogenesis. | ASA may promote the resolution of inflammation via the production of lipoxin A4 [158, 159]. |
Remyelination | Remyelination is incomplete in MS [212]. | ASA may increase ciliary neurotrophic factor and promote the differentiation and proliferation of oligodendrocyte precursors [161, 163]. |
Fatigue | Fatigue is a common symptom of MS. | ASA may reduce fatigue in MS patients via antipyretic effects or by countering proinflammatory cytokines [164, 176, 177]. |
Depression | Depression is more common in MS than in the general population [180]. | ASA usage may lower the risk for major depression, and some evidence shows that ASA in combination with fluoxetine enhances treatment for depression [181, 182, 188]. It is unknown whether ASA would help to reduce depression in MS, but other studies suggest that it can have negative impacts or side effects in depressed patients (see Table 2) |
General disease activity | MS patients given calcium aspirin (Solprin) [147, 148] or EAE subjects given sodium salicylate or ASA [149–152]. Studies were performed decades ago. | Overall, the outcome is inconclusive. There was no effect in MS patients [147, 148], but evaluation was done using an outdated measure of disease activity. In EAE, disease onset was delayed and/or disease incidence reduced in 3 out of 4 studies [149, 151, 152]. Treatment after clinical signs appeared resulted in no benefit [149], and in one study disease severity was increased although disease onset was delayed [151]. |