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Evaluates cognitive function during evolocumab treatment for elevated cholesterol, highlighting potential risks linked to low circulating cholesterol levels.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates levels of plasma LDL-C by interacting with the LDL receptor. After binding and internalization, PCSK9 directs the LDL receptor to lysosomal degradation and inhibits its recycling to the cell surface, and thus accelerates the degradation of hepatic LDL receptors. This reduces the capacity of the liver to remove LDL-C from the circulation. Evolocumab, a monoclonal antibody against PCSK9, substantially reduces LDL-C levels. However, given the importance of cholesterol in synapse formation and function, the potential adverse cognitive effects of cholesterol-reducing drugs are a reasonable concern, particularly in the case of lipophilic statins that are able to cross the blood–brain barrier.14 Data from several sources have suggested that low levels of either LDL-C or the monoclonal antibodies may be associated with impaired cognitive function.
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Rp et al. (2018) studied this question.
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