Cholesterol Management in Neurology: Time for Revised Strategies?

Abstract

Statin therapy has been extensively evaluated and shown to reduce the incidence of new or recurrent vascular events, ischemic stroke included. As a consequence, each published guideline pushes for lower low-density cholesterol levels in the population at large, recommending increased statin doses and/or adding new cholesterol-lowering molecules. Neurologists find it sometimes difficult to apply these guidelines, having to confront situations such as (1) ischemic strokes, mainly cardioembolic ones, in patients with already low LDL-cholesterol levels; (2) myasthenic patients, whose lifespan has been extended by available treatment, and whose age and cholesterol levels put them at risk for ischemic stroke; (3) patients with myotonic dystrophy, whose disease often associates diabetes mellitus and heart conduction defects, and in whom blood cholesterol management is also not settled. As such, further trials are needed to address these issues.

Early postoperative cognitive decline—are there any preventive strategies for surgical patients in the emergency setting?

“…In regard to antioxidative therapy, statins have been proposed to be valuable in improving neurocognitive disorders including both dementia and postoperative delirium, due to its ability to reduce the levels of oxidative species [38,39]. Although currently there are no clinical studies underway to investigate this favourable result of statins, previous randomized controlled trials demonstrated a significant reduction on early postoperative memory impairment by using statin therapy [39,40].…”

The Involvement of Neuroinflammation in the Onset and Progression of Parkinson’s Disease

“…In an experimental setting, DJ-1 knockdown exacerbated rotenone-induced impairments of mitochondrial fission [187], led to increased nitrative stress [188], and to increased production of COX-2 and IL-6 after LPS treatment [189]. DJ-1 also associates with lipid rafts [190], cholesterol-enriched membrane domains with a crucial role in synaptic transmission, endoand exocytosis, as well as signal transduction [191]. The astrocytic dysregulation of the inflammatory response appears to be related to TLR4 receptors, DJ-1 knockout astrocytes having impaired lipid raft assembly leading to impaired TLR4 endocytosis [192].…”