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Amyloid-beta is a toxic 42-amino acid peptide that clumps and forms plaques in the brain with age. Amyloid-beta is associated with Alzheimer’s disease, a progressive neurodegenerative disease and the most common cause of dementia. Findings from a new study demonstrate that sulforaphane impairs BACE1, an enzyme involved in the production of amyloid-beta.
BACE1, or beta site amyloid precursor protein cleaving enzyme 1, is produced primarily in the central nervous system. People with Alzheimer’s disease often have high levels of BACE1 in their brains.
The authors of the study set out to evaluate sulforaphane’s capacity to inhibit BACE1. They used fluorescence resonance energy transfer analysis to determine the enzyme’s activity and then calculated its kinetics. They assessed sulforaphane’s enzyme selectivity in the presence of several other enzymes and compared its effects to those of resveratrol and quercetin, bioactive compounds that exert beneficial effects on human health.
They found that sulforaphane was six times more effective against BACE1 compared to resveratrol and quercetin. Sulforaphane demonstrated high affinity for BACE1 and had few off-target effects, suggesting that sulforaphane shows promise as a candidate to reduce the activity of BACE1, potentially playing a role in preventing Alzheimer’s disease.
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