Fisetin became the focus of investigations when researchers discovered a positive correlation between strawberry consumption and mental functioning. Since research has shown that fisetin has neurotrophic, anti-cancer, anti-inflammatory, anti-oxidant effects and may protect against cognitive and neurological disorders such as Alzheimer’s disease.
Last month a research team largely comprised of members of the Gyeongsang National University in Korea released findings showing the neuroprotective effect of fisetin against amyloid-beta (Aβ) induced cognitive/synaptic dysfunction, neuroinflammation and neurodegeneration in adult mice.
The exact molecular mechanism of Alzheimer’s disease is still unproven, but Alzheimer’s disease is probably caused by complex interactions among several contributing factors, such as genetics, oxidative stress, and inflammatory and environmental factors. A growing body of evidence suggests that the disease is characterized by the accumulation of amyloid beta and the hyperphosphorylation of tau proteins in the brain. This deposition of amyloid-beta (Aβ) peptides (Aβ1–42) triggers synaptic dysfunction, hyperphosphorylation of tau and (apoptotic) neurodegeneration which eventually lead to cognitive deficits and progression of Alzheimer’s disease (AD).
The researchers designed the study to investigate the neuroprotective effects of fisetin against this Aβ 1–42 induced cognitive deficits, neuroinflammation, and neurodegeneration in the adult mouse hippocampus.
They created 3 groups of mice:
1) A healthy control group
2) A mice group with Aβ 1–42 injected peptides that leads to the Alzheimer’s disease pattern
3) A mice group with the Aβ 1–42 injected peptides but these mice received treatments with fisetin, injected daily (20mg/kg) for a two weeks period.
Testing with the different groups showed that Fisetin: reverses Aβ 1–42 induced memory dysfunction, protects against Aβ 1–42 induced synaptic dysfunction, abrogates Aβ 1–42 induced suppression of PI3K/Akt/GSK3β signaling, attenuates inflammatory mediators and gliosis and prevents Aβ 1–42 induced apoptotic neurodegeneration.
Overall these findings suggest that fisetin treatment significantly reduces Aβ deposition, tau hyperphosphorylation, and synaptic dysfunctions while also enhancing memory function in the used mouse model of Alzheimer’s disease. In addition it was found that fisetin treatment regulates the neuronal survival signaling pathways and significantly prevents neuroinflammation and apoptotic neurodegeneration in the adult mouse hippo-campus.
This adds to the evidence that flavonoids such as fisetin, could be safe candidates for preventing and halting progressive and age related neurological disorders such as Alzheimer’s disease. A study of the Salk Institute found that adding fisetin to food supported memory and learning skills.