Alzheimer's Disease (AD) and other neurodegenerative diseases, involve a complex etiology in both the initiation and progression of the disease. In AD known disease factors involve amyloid plaques, neurotangles (fibrils), inflammation and oxidative stress. Further research into this disease indicates that glycation of the amyloid, neurotangles and neurons may dramatically escalate destruction of the brain and accelerate disease progression. Mitigating glycation in the brain provides another target in the prevention of neurodegenerative diseases.
SULFORAPHANE targets the effects of oxidative stress and inflammation, both dominating factors in degenerative brain disease, including reduction of damage attributed to the damaging glycation. Glycation of proteins, which occurs by the irreversible attachment of sugar to causes an accumulation of damaged brain proteins and is believed to be an important causative factor in AD.(1)
Methylglyoxal (MG) - the role in Alzheimer's Disease. Glycated proteins lead to the formation of toxic Advanced Glycation Endproducts (AGEs) and are a significant source of inflammation. AGEs are found in high amounts in the brains of Alzheimer's patients in conjunction with amyloid plaques and neurotangles.Methylglyoxal (MD) is a potent precursor of AGEs and is directly responsible for increased oxidative stress and deterioration of brain function.
Sulforaphane increases cellular protection and enhances Methylglyoxal breakdown. Sulforaphane protects the brain by multiple paths.
- Increases critical levels of intracellular glutathione -offering significant protection to the neurons including reduction of neuron death.
- Increases breakdown of MG by elevating enzyme glyoxalase activity.
- Increases Brain Derived Neurotrophic Factor (BDNF). BDFN, which is neuro protective, and is reduced in AD patients. Lower BDNF levels are considered a biomarker for Alzheimer's.
- Maintains critical glucose uptake for neuron energy. Methylglyoxal blocks important glucose uptake by the neurons which is totally reversed by sulforaphane. When neurons are deprived of glucose (their main energy source) they can not survive.
- Sulforaphane also is an inhibitory of neuroinflammation. Using human micro-glia like cells, sulforaphane has been shown to inhibit the proinflammatory cascade triggered by beta-amyloid peptides, thereby significantly reducing damaging inflammation occurring in the AD brain.(2)
XGEVITY (Glucoraphanin precursor to Sulforaphane)
(1) Angeloni C, et al. Antiglycative activity of sulforaphane: a new avenue to counteract neurodegeneration? Neural Regen Res. 2015 Nov.
(2) An YW, et al. Sulforaphane exerts its anti-inflammatory effect against amyloid-β peptide via STAT-1 dephosphorylation and activation of Nrf2/HO-1 cascade in human THP-1 macrophages. Neurobiol Aging 2016 Feb;