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Alzheimer’s disease: A food to improve cognitive function

By Tucson Functional Medicine on July 11, 2022 0 Comments

Walnuts have been shown to improve memory, cognition, and neuronal effects related to oxidative stress (OS) and inflammation (INF) in animals and human trials.

Walnut looks like the brain and has a left and right hemisphere, upper cerebrum, and lower cerebellum. The folds and wrinkles of a walnut resemble the human organ: the brain. The shape of the nut even approximates the body part, looking like it has left and right hemispheres. And it’s no surprise walnuts are nicknamed “brain food”—they have a very high content of omega-3 fatty acids, which help support brain function.” The wrinkles and folds mimic the neo-cortex

 

Walnuts develop over three dozen neuron transmitters for brain function. They may also help head off dementia. A recent study found that walnut extract broke down the protein-based plaques associated with Alzheimer’s disease. In addition, they found walnuts reversed some signs of brain aging in rats. Walnuts also appear to enhance signaling within the brain and encourage new messaging links between brain cells.

Fibrillar amyloid beta-protein (Abeta) is the principal component of amyloid plaques in the brains of patients with Alzheimer’s disease. Scientific studies suggest that walnuts may reduce the risk or delay the onset of Alzheimer’s disease by maintaining Abeta in the soluble form. In addition, walnuts had inhibited Abeta fibrillization. It is proposed that polyphenolic compounds (such as flavonoids) present in walnuts may be responsible for their anti-amyloidogenic activity.

References:

Poulose SM1, Miller MG, Shukitt-Hale B., Role of walnuts in maintaining brain health with age. J Nutr. 2014 Apr;144

Poulose SM1, Bielinski DF, Shukitt-Hale B. Walnut diet reduces the accumulation of polyubiquitinated proteins and inflammation in the brain of aged rats. J Nutr Biochem. 2013 May;24(5):912-9

Chauhan N1, Wang KC, Wegiel J, Malik MN. Walnut extract inhibits the amyloid beta protein’s fibrillization and defibrillizes its preformed fibrils. Curr Alzheimer Res. 2004 Aug;1(3):183-8.

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