Title: Neurodegeneration: Mechanisms, pathways and therapeutic actions.
Speaker: Jon Lozier, DC
Live Class (June 2018) Video with Slides – 2 CEU
Neurodegeneration use the slow and long-term Loss of neurons as a result of oxidative damage. Many of the mechanisms behind diseases such as Parkinson’s disease, Alzheimer's disease, and even multiple sclerosis and amyotrophic lateral sclerosis are becoming more clearly understood. Further, there is good and scientific literature suggesting that these poses sees can be slowed down or even reversed in some cases by way of nutritional support. This lecture lays out the case for Neurodegeneration due to oxidative damage, discusses biochemical pathways that may be involved, and suggests nutritional therapeutics.
Objectives:
Define Neurodegeneration.
Identify some of the core mechanisms of Neurodegeneration.
Define and discuss oxidative stress and damage of neurons.
List most common neurological illnesses thought to be due to long-term Neurodegeneration.
Cite specific biochemical pathways to target therapeutically to slow down or reverse Neurodegeneration.
Itemize common clinical findings in Parkinson’s disease, Alzheimer's disease, and multiple sclerosis.
List the mechanisms involved in the neurodegenerative process.
Define free radicals, articulate the issue with free radicals and describe their role in the neurodegenerative process.
Discuss the role of glial cells in regard to Neurodegeneration.
Itemize ways to increase the Nrf2 pathway.
Discuss glutathione and list specific methods to increase glutathione levels.
List dangers found in regard to genetically modified foods.
Compare and contrast normal mitochondrial structure and function with dysfunctional mitochondria with attention to free radical damage to my no conjugal proteins and mitochondrial DNA.
Discuss the therapeutic role of essential fatty acids (EFA's), Acetyl-L-Carnitine, and coenzyme Q-10.
List and discuss methods for laboratory evaluation of systemic inflammation.
Itemize issues associated with the "leaky gut" syndrome, including aspects of inflammation, relation to diabetes, and Zonulin.
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