Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer's Disease

Int J Mol Sci. 2021 Mar 13;22(6):2929. doi: 10.3390/ijms22062929.

Abstract

Sulforaphane, a potent dietary bioactive agent obtainable from cruciferous vegetables, has been extensively studied for its effects in disease prevention and therapy. Sulforaphane potently induces transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated expression of detoxification, anti-oxidation, and immune system-modulating enzymes, and possibly acts as an anti-carcinogenic agent. Several clinical trials are in progress to study the effect of diverse types of cruciferous vegetables and sulforaphane on prostate cancer, breast cancer, lung cancer, atopic asthmatics, skin aging, dermatitis, obesity, etc. Recently, the protective effects of sulforaphane on brain health were also considerably studied, where the studies have further extended to several neurological diseases, including Alzheimer's disease (AD), Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, autism spectrum disorder, and schizophrenia. Animal and cell studies that employ sulforaphane against memory impairment and AD-related pre-clinical biomarkers on amyloid-β, tau, inflammation, oxidative stress, and neurodegeneration are summarized, and plausible neuroprotective mechanisms of sulforaphane to help prevent AD are discussed. The increase in pre-clinical evidences consistently suggests that sulforaphane has a multi-faceted neuroprotective effect on AD pathophysiology. The anti-AD-like evidence of sulforaphane seen in cells and animals indicates the need to pursue sulforaphane research for relevant biomarkers in AD pre-symptomatic populations.

Keywords: Alzheimer’s disease; amyloid-β; inflammation; memory; neurodegeneration; oxidative stress; sulforaphane; tau.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Peptides / antagonists & inhibitors
  • Amyloid beta-Peptides / genetics*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Biomarkers / metabolism
  • Cell Line, Tumor
  • Disease Models, Animal
  • Drug Administration Schedule
  • Drug Evaluation, Preclinical
  • Gene Expression Regulation
  • Humans
  • Isothiocyanates / pharmacology*
  • Memory Disorders / genetics
  • Memory Disorders / metabolism
  • Memory Disorders / physiopathology
  • Memory Disorders / prevention & control*
  • Neurons / drug effects
  • Neurons / metabolism
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects
  • Protein Aggregates / drug effects
  • Protein Aggregates / genetics
  • Sulfoxides / pharmacology*
  • tau Proteins / antagonists & inhibitors
  • tau Proteins / genetics*
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Biomarkers
  • Isothiocyanates
  • MAPT protein, human
  • Neuroprotective Agents
  • Protein Aggregates
  • Sulfoxides
  • tau Proteins
  • sulforaphane