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Intensive LDL-cholesterol lowering therapy and neurocognitive function.

Maciej Banach1, Manfredi Rizzo2, Dragana Nikolic3

  • 1Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Leodz, Poland; Healthy Aging Research Centre (HARC), Medical University of Lodz, Lodz, Poland; Polish Mother's Memorial Hospital Research Institute, Lodz, Poland.

Pharmacology & Therapeutics
|November 21, 2016
PubMed
Summary

Lipid-lowering drugs like statins and PCSK9 inhibitors aim to reduce cardiovascular risk. Current evidence on their impact on neurocognition, including memory loss and dementia, remains inconclusive, necessitating further research.

Keywords:
Lipid-lowering drugsLow-density lipoprotein cholesterolNeurocognitive functionProprotein convertase subtilisin/kexin type 9Statins

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Area of Science:

  • Cardiovascular Medicine
  • Neuroscience
  • Pharmacology

Background:

  • Guideline-recommended low-density lipoprotein cholesterol (LDL-C) reduction is crucial for cardiovascular disease (CVD) prevention, primarily achieved with statins.
  • Novel therapies like proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors offer advanced lipid-lowering strategies to mitigate residual CVD risk.
  • Concerns have been raised by regulatory bodies regarding potential neurocognitive adverse effects associated with these lipid-lowering agents.

Purpose of the Study:

  • To review the current, often conflicting, evidence regarding the association between statin use and cognitive function.
  • To explore the potential impact of intensive LDL-C lowering, including newer agents, on neurocognition.
  • To identify factors that may influence susceptibility to cognitive changes during lipid-lowering therapy.

Main Methods:

  • Systematic review and critical analysis of existing clinical studies and scientific literature.
  • Evaluation of evidence for both cognitive impairment and potential benefits, such as dementia prevention.
  • Consideration of confounding factors including pre-existing conditions, genetics (e.g., APOE ε-4), and aging.

Main Results:

  • Evidence linking statins to clinically significant cognitive impairment is disputed, with some studies suggesting memory loss and others indicating a protective effect against dementia.
  • The impact of intensive LDL-C lowering on neurocognition may involve off-target effects or be influenced by underlying pathologies.
  • Individual susceptibility to cognitive effects may be modulated by genetic factors, lipid profiles (apoA1, HDL-C), and age.

Conclusions:

  • The current debate on statins and cognition should not impede appropriate lipid-lowering therapy, but prescribers must remain vigilant for potential side effects.
  • Further prospective, controlled studies are essential to elucidate the short- and long-term effects of various lipid-lowering drugs on cognitive function.
  • Future research requires rigorous design to disentangle the complex interplay between lipid levels, genetic predispositions, and neurocognitive outcomes.