Fingolimod Reduces Alzheimer’s Disease Pathological Features in Mouse Model

Fingolimod Reduces Alzheimer’s Disease Pathological Features in Mouse Model
Researchers tested the effects of fingolimod, an approved treatment for multiple sclerosis shown to have anti-inflammatory properties, in a mouse model of Alzheimer’s disease (AD). The drug reduced the density of pathological plaques and decreased the number of pro-inflammatory cells in in vivo disease models, suggesting a potential therapeutic role for Alzheimer's. The research paper, “Fingolimod modulates multiple neuroinflammatory markers in a mouse model of Alzheimer’s disease,” was published in Scientific Reports. Plaque deposits of insoluble, aggregated amyloid β (Aβ) peptide is one of the most important neuropathological hallmarks of Alzheimer’s disease, and its neurotoxicity has been correlated with neuronal and synaptic loss, which leads to the decline in cognitive function observed in Alzheimer’s patients. These events are accompanied by neuroinflammatory reactions that have been attributed to reactive astrocytes and abnormally activated microglial cells, which in normal circumstances act as the main immune defenses in the central nervous system (CNS), but in Alzheimer’s patients, are thought to turn against healthy tissue and are present in high levels among amyloid plaques. Immunomodulating drug fingolimod is a functional sphingosine 1-phosphate (S1P) receptor antagonist shown to have anti-inflammatory properties, preventing the migration of lymphocytes into the CNS and with a possible protective effect against neuroinflammation. Moreover, the compound is able the cross the blood-brain-barrier, therefore having a potential effect on CNS cells
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