Parkinson’s Disease Explained

The Problem
Parkinson’s disease is like Alzheimer’s disease in that it is associated with aggregated proteins in the brain, but now initially affecting motor skills instead of loss of memory.  Furthermore, like Alzheimer’s disease, there appears to be a link between insulin resistance and Parkinson’s (22).  In addition, the relationship between decreased AMPK activity and Parkinson’s is also quite strong  (23).  Finally, disruption of AMPK activity in dopamine-associated neurons promotes Parkinson’s-like symptoms (24).

The longer the Parkinson’s patient survives, their mental skills begin to erode as the neuroinflammation spreads to the cognitive areas of the brain.  Also, like Alzheimer’s disease, advanced Parkinson’s disease is associated with aggregated protein clumps known as Lewy bodies. The removal of such protein aggregates is mediated by autophagy, which is controlled by AMPK activity (24).  In essence, the progression of Parkinson’s disease may be better understood as an AMPK inhibition condition. 

The Traditional Medical Approach
The primary drug used to treat Parkinson’s is L-dopa, which is the precursor to dopamine.  Unfortunately, the benefits of L-dopa fall off after a few years, and the progression of Parkinson’s continues.

The Metabolic Engineering® Approach
The best way to increase the energy production of mitochondria in the brain (as well as every cell in the body) is to activate AMPK. The most effective tool to do that is following Metabolic Engineering® at the first sign of increasing insulin resistance. 

The goal of Metabolic Engineering® is to activate AMPK in the brain.  Using the Zone diet component of Metabolic Engineering® to restrict calories without hunger or fatigue is the most powerful dietary approach for increasing AMPK activity.  The omega-3 fatty acid dietary component of Metabolic Engineering® reduces neuroinflammation and promotes its resolution.  The polyphenol dietary component of Metabolic Engineering® reduces oxidative stress.  Equally important is that the omega-3 fatty acid and polyphenol components of Metabolic Engineering® are also indirect activators of AMPK activity.   Thus, combining all three dietary interventions in Metabolic Engineering® provides the optimal dietary approach to maximizing AMPK activity to reduce neuroinflammation. 

As with Alzheimer’s, the increase in insulin resistance will occur years ahead of the development of the symptoms of Parkinson’s disease. Thus, the best way to reduce the likelihood of developing Parkinson’s disease is to reduce, if not eliminate, insulin resistance as early as possible.

References 
1. Sharma T, Kaur D, Grewal AK, Singh TG.Therapies modulating insulin resistance in Parkinson’s disease: A cross-talk.  Neurosci Lett. 2021 Apr 1;749:135754.doi: 10.1016/j.neulet.2021.135754.

2. Curry DW, Stutz B, Andrews ZB, Elsworth JD.Targeting AMPK signaling as a neuroprotective strategy in Parkinson’s disease.  J Parkinsons Dis. 2018; 8:161-181. doi: 10.3233/JPD-171296.

3. Parekh P, Sharma N, Sharma M, Gadepalli A, Sayyed AA, Chatterjee S, Kate A, Khairnar A.AMPK-dependent autophagy activation and alpha-Synuclein clearance: a putative mechanism behind alpha-mangostin’s neuroprotection in a rotenone-induced mouse model of Parkinson’s disease.  Metab Brain Dis. 2022; 37:2853-2870. doi: 10.1007/s11011-022-01087-1.

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