The general notion is that deposition of beta-amyloid (Aβ) peptides in senile plaques is the characteristic feature of the Alzheimer's disease progression. In a recent study it was found that Pinocembrin may be a useful drug in the treatment of Alzheimer's disease.
The actual etiology of Alzheimer's disease is not clearly known and is still debatable.
AdvertisementHowever it is widely believed that 'the accumulation of beta-amyloid (Aβ) peptides in the senile plaques is one of the hallmarks of the progression of the disease.'
The neural degeneration associated with Alzheimer's disease (AD) is affected by interaction between Aβ and a receptor called receptor for advanced glycation end products (RAGE).
'Pinocembrin is a flavanone, a type of flavonoid. It is an antioxidant found in damiana, honey, and propolis.'
Rui Liu et al published a study in BMC Medicine 2012 based on their findings that pinocembrin protects against beta-amyloid-induced toxicity in neurons through inhibiting receptor for advanced glycation end products (RAGE).
Various health promoting biological activities are attributed to the presence of pinocembrin. Earlier researches have revealed the neuroprotective effects of pinocembrin particularly in cases of vascular and ischemic dementia in animals.
Since State Food and Drug Administration of China approved pinocembrin for being used in stroke patients, it has been examined for improving cognitive functions and neuronal protection against toxicity induced by Aβ.
For the purpose of study, pinocembrin was administrated orally in a dose of 20 mg/kg/day and 40 mg/kg/day for 8 days in mice treated with Aβ 25-35 to induce Alzheimer-like changes. Brain changes were evaluated based on analysis of neuronal degeneration, behavioral performance and cerebral cortex neuropil ultrastructure, and RAGE expression.
The researchers discovered that pinocembrin, if administered orally, can improve cognitive function and decrease the neurodegeneration of cerebral cortex in Aβ 25-35treated mice. Pinocembrin remarkably reduced the upregulation of receptor for advanced glycation end products (RAGE). It also reduced the inflammatory response consequent of Aβ-RAGE interaction.
Further, pinocembrin improved dysfunctioning of mitochondria by enhancing mitochondrial potential and reducing oxidative stress of mitochondria.
The scientists concluded that pinocembrin improved neuronal protection and may prove to be an important candidate for treating Alzheimer's disease.
Pinocembrin protects against beta-amyloid-induced toxicity in neurons through inhibiting receptor for advanced glycation end products (RAGE)-independent signaling pathways and regulating mitochondrion-mediated apoptosis; Rui Liu et al; BMC Medicine 2012
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