Fibrillar amyloid beta-protein (Aβ) is the principal component of amyloid plaques in the brains of patients with Alzheimers disease. We have studied the effect of walnut extract on Aß fibrillization by Thioflavin T fluorescence spectroscopy and electron microscopy. The walnut extract not only inhibited Aß fibril formation in a concentration and time- dependent manner but it was also able to defibrillize Aβ preformed fibrils. Over 90% inhibition of Aβ fibrillization was observed with 5 ml of methanolic extract of walnut (MEOW) both after 2 and 3 days of incubation. The maximum defibrillization (91.6%) was observed when preformed Aβ fibrils were incubated with 10 ml of MEOW for 2 days. These results suggest that walnuts may reduce the risk or delay the onset of Alzheimers disease by maintaining Aß in the soluble form. Further studies showed that anti-amyloidogenic compound in walnut is an organic compound of molecular weight less than 10 kDa, which is neither a lipid nor a protein. Chloroform extract of walnut had no effect on Aβ fibrillization while MEOW and its 10 kDa filtrate inhibited Aβ fibrillization equally. It is proposed that polyphenolic compounds (such as flavonoids) present in walnuts may be responsible for its anti-amyloidogenic activity.
Keywords: alzheimer disease, amyloid beta-protein, beta-amyloidosis, fibrillization, walnut
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