Walnut Extract Inhibits the Fibrillization of Amyloid Beta-Protein, and also Defibrillizes its Preformed Fibrils

Abstract

Fibrillar amyloid beta-protein (Abeta) is the principal component of amyloid plaques in the brains of patients with Alzheimer's disease. We have studied the effect of walnut extract on Abeta fibrillization by Thioflavin T fluorescence spectroscopy and electron microscopy. The walnut extract not only inhibited Abeta fibril formation in a concentration and time- dependent manner but it was also able to defibrillize Abeta preformed fibrils. Over 90% inhibition of Abeta fibrillization was observed with 5 microl of methanolic extract of walnut (MEOW) both after 2 and 3 days of incubation. The maximum defibrillization (91.6%) was observed when preformed Abeta fibrils were incubated with 10 microl of MEOW for 2 days. These results suggest that walnuts may reduce the risk or delay the onset of Alzheimer's disease by maintaining Abeta 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 Abeta fibrillization while MEOW and its 10 kDa filtrate inhibited Abeta fibrillization equally. It is proposed that polyphenolic compounds (such as flavonoids) present in walnuts may be responsible for its anti-amyloidogenic activity.

Walnut Extract Inhibits LPS-induced Activation of Bv-2 Microglia via Internalization of TLR4: Possible Involvement of Phospholipase D2

“…Methanolic extract of walnut was prepared according to previously published methods [17]. Briefly, 4 g of English walnuts (J. regia, California Walnut Commission) were homogenized in 10 ml of methanol and centrifuged at 17,000 g for 5 min.…”

“…Cells were pre-treated with either walnut extract in media or control media overnight and then stimulated with LPS (Sigma-Aldrich, MO, USA) at 100 ng/ml overnight. Walnut extract concentrations ranged from 0.00001 to 10 mg of walnuts per milliliter of solution, based on previous studies by Chauhan et al [17]. For experiments involving n-butanol, cells were pre-treated with control media or walnut extract plus 0.3% n-butanol (Sigma-Aldrich, MO, USA), followed by overnight exposure to LPS.…”

A cross sectional study of the association between walnut consumption and cognitive function among adult us populations represented in NHANES

“…Amyloid beta-protein is the principal component of amyloid plaques in the brains of patients with AD (13). In cell lines, walnut extract reduces amyloid beta protein-induced oxidative stress and cell death (13,14). These research findings suggest that a diet rich in walnuts may help prevent and delay the onset of AD (12,14).…”

“…Amyloid beta-protein is the principal component of amyloid plaques in the brains of patients with AD (13). In cell lines, walnut extract reduces amyloid beta protein-induced oxidative stress and cell death (13,14).…”

Cholesterol Homeostasis Imbalance and Brain Functioning: Neurological Disorders and Behavioral Consequences

“…Chronic simvastatin application is able to lower Aβ in the CSF of guinea pigs, whereas the discontinuation of the pharmacological treatment reverses this effect [41]. Similarly, lovastatin and pravastatin administrations reduce Aβ levels in transgenic mice [57]. Although human studies display variable outcomes, clinical evidence is encouraging, suggesting that statin therapy could be a valuable pharmacological strategy to treat AD patients.…”