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Parkinson's, Alzheimer's, and the New Science of Hope

ByCrossFitJanuary 3, 2020

In this 2019 piece for Psychology Today, Georgia Ede summarizes the potential role metabolic defects in the brain may have in the development and progression of Alzheimer’s disease (AD) and Parkinson’s disease (PD).

In both AD and PD, defective brain glucose metabolism leads to brain cell dysfunction and death. In AD, this defect begins in the hippocampus, which controls memory function; in PD, the substantia nigra, which controls movement coordination, deteriorates first. Both are among the most glucose-hungry regions of the brain and are therefore uniquely sensitive to metabolic defects. Impaired insulin sensitivity in the brain (described in detail previously on can cause these defects by preventing insulin from crossing the blood-brain barrier, thereby degrading the metabolic capacity of brain cells even when glucose remains available.

Multiple studies have begun to suggest insulin resistance plays a role in PD progression. More than half of PD patients are insulin resistant, and those who are insulin resistant tend to have more severe symptoms and faster disease progression than those who are not (1). AD has similarly been theorized to have a link to insulin resistance (as previously discussed on, with some going so far as to call it “Type 3 diabetes.”

Two small pilot trials have tested a ketogenic diet (KD) in PD patients. A small 2005 pilot study (2) observed improvements according to a scale measuring PD symptom severity (3) when patients followed a KD, though this may have been due to a diet-drug interaction. A 2018 trial (4) found PD patients who followed a KD demonstrated improvements in nonmotor daily living experiences, though there were no significant improvements in motor control.

These preliminary data suggest insulin resistance in the brain, or some other metabolic defect, may play a role in AD and PD progression. Additional research is needed to understand the clinical significance of these observations.

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