Neuroprotective Mechanisms of Polyphenols in Alzheimer's Disease
Summary
Polyphenols exert multifaceted neuroprotective effects that target core pathological features of Alzheimer’s disease (AD). These naturally occurring phytochemicals counteract oxidative stress by scavenging reactive oxygen species and up-regulating endogenous antioxidant enzymes. They attenuate neuroinflammation through inhibition of pro-inflammatory cytokine release, suppression of microglial activation and interference with inflammasome assembly. Polyphenols also modulate amyloid-β metabolism, promoting its clearance via proteasomal degradation and autophagy, whilst reducing peptide aggregation. Beyond these canonical pathways, certain polyphenols activate metabolic sensors such as SIRT1 and AMP-activated protein kinase, thereby enhancing mitochondrial function and triggering epigenetic programmes that bolster neuronal resilience. Interactions with gut microbiota and the blood-brain barrier further shape their bioavailability and efficacy. Collectively, these mechanisms underpin the potential of dietary polyphenols and their derivatives as adjunctive strategies to delay cognitive decline and complement existing therapeutic approaches on a global scale.
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Neuroprotective Mechanisms of Polyphenols in Alzheimer's Disease publication trend
The graph below shows the total number of articles in neuroprotective mechanisms of polyphenols in alzheimer's disease across all publications each year (not limited to Nature Index journals).
Technical terms
Amyloid-β peptides: Short fragments of the amyloid precursor protein that aggregate into plaques, a hallmark of Alzheimer’s pathology.
Neuroinflammation: Inflammatory response within the central nervous system primarily mediated by activated glial cells, contributing to neuronal damage.
NLRP3 inflammasome: A multiprotein complex in microglia and other immune cells that triggers production of pro-inflammatory cytokines upon activation.
SIRT1: A NAD⁺-dependent deacetylase that regulates stress resistance, mitochondrial function and gene expression linked to cellular longevity.
Autophagy: A lysosome-mediated degradation pathway that clears damaged organelles and aggregated proteins to maintain neuronal homeostasis.
Decoy receptor: A membrane-bound or soluble receptor that binds inflammatory ligands without transducing a signal, thereby limiting inflammatory cascades.
References
- Resveratrol Activates Antioxidant Protective Mechanisms in Cellular Models of Alzheimer’s Disease Inflammation. Antioxidants (2024).
- Decoy Receptors Regulation by Resveratrol in Lipopolysaccharide-Activated Microglia. Cells (2023).
- The pleiotropic neuroprotective effects of resveratrol in cognitive decline and Alzheimer’s disease pathology: From antioxidant to epigenetic therapy. Ageing Research Reviews (2021).
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