Course Description
Course Fee: $255
Instructor: James Greenblatt, MD
This three-module course presented by Dr. James Greenblatt presents a novel paradigm for the prevention of Alzheimer’s, as well as general cognitive decline. It examines the pathophysiology of neurodegenerative illness from a functional medicine and systems biology framework, focusing on biochemical abnormalities contributing to neuronal dysfunction that are modifiable at certain prodromal stages…and, accordingly, viable functional treatment targets. Research supporting the use
of low-dose lithium and other evidence-based nutritional interventions as part of a preventative approach will be objectively reviewed, and the mechanisms through which these interventions confer neuroprotection elucidated.
Finally, evidence-based recommendations for the use of low-dose lithium and other functional medicine treatments will be proffered, providing students with actionable information that can be incorporated into existing treatment protocols to maximize therapeutic – and cognitive – outcomes.
Learning Objectives
Upon completion of this course, students will be able to:
- Describe one way in which high homocysteine is related to risk for Alzheimer’s
- List three OPCs and describe how they may impact brain health
- Explain what each of the letters in the ZEEBRA model stands for, as an approach to treating Alzheimer’s and cognitive decline
Modules
Module 1
- An Overview of Neurodegenerative Illness
a. Epidemiology, presentation
b. Pathophysiology - The Search for A Cure
a. Investments, failures from Big Pharma - The Alzheimer’s prodrome: paradigm-altering implications
- Lithium
a. An essential, natural micronutrient
b. Neuroprotective properties
c. Research evidence: the Tap Water Studies
d. Elucidating dose: from nutritional to pharmaceutical
e. Research evidence: insights from Bipolar
f. Honing in on lithium’s utility for Alzheimer’s: when and how much matters!
g. Lithium as part of a preventative approach: hope on the horizon
h. Lithium mechanisms, effects on neurotransmission, inhibition of GSK-3, optimization of BDNF activity/expression
i. Lithium for irritability, agitation
j. Lithium for Parkinson’s - Elucidating a functional psychiatry model for Alzheimer’s prevention
Module 2
-
- Homocysteine: A Modifiable Alzheimer’s Risk Factor
a. International consensus on risk
b. Mechanisms; exploring the relationship between HCy and Vitamin B12 - Vitamin B9 (Folate)
a. Folic acid vs. folate vs. L-methylfolate
b. Folate risk deficiency factors
c. Genetic risk factors: MTHFR polymorphisms - Vitamin B12
a. B12 deficiency: illuminating physical and neurologic symptoms
b. B12 to mitigate high HCy
c. Mechanisms of neuroprotection; influences on neurotransmission
d. Risk factors for B12 deficiency - Vitamin B6 (pyridoxine)
a. An essential cofactor: B6 functions
b. Exploring B6 and cognitive decline: the research
c. Pyroluria (Overview, clinical implications, testing, treatment) - Vitamin B2 (riboflavin)
a. Overview, function
b. Associations with cognitive decline - Vitamin B3 (niacin)
a. Illuminating B3’s importance: the history of pellagra
b. Niacin therapy: applications across diagnoses
c. Formulations, roles, biologic activity
d. Effects on cellular energy production, neurotransmission
e. Evidence supporting B3/nicotinamide as a treatment for Alzheimer’s - Vitamin D
a. Categorization, functions
b. Role in neurotransmission
c. Homeostatic controls: vitamin D and serotonin synthesis/regulation
d. Vitamin D and gene expression
e. Hypovitaminosis D: A global phenomenon
– Contributing factors
– Establishing laboratory values for insufficiency, deficiency, sufficiency
– The importance of testing
– Diet and vitamin D
– Vitamin D, aging, and Alzheimer’s: the research
– Elucidating critical windows for prevention
– Magnesium and vitamin D activation
- Homocysteine: A Modifiable Alzheimer’s Risk Factor
Module 3
-
- Oligomeric Proanthocyanidins (OPCs)
a. Classification – phenols
b. Neuroprotective effects
– Enzyme modulation/reuptake
– Influences on neurotransmission
c. Illuminating potential health benefits + clinical applications
d. Mechanisms
e. OPCs for brain health, cognition: the research - N-Acetyl Cysteine (NAC)
a. Antioxidant mechanisms, activity
b. NAC and Alzheimer’s: research-supported connections
c. Potential mechanisms of neuroprotection - Curcumin
a. Classification, distribution, tradition of medicinal usage
b. Pharmacologic properties
c. Proposed antidepressant mechanisms
d. Documented neuroprotective mechanisms
e. Case studies
e. Experimental studies, clinical trials
f. Anti-inflammatory, antioxidant properties
g. Factors influencing bioavailability
h. Curcumin + vitamin D - Creatinine
a. Associations with dementia, Alzheimer’s - Chromium
a. Biologic roles, influences on energy balance and neurotransmission
b. Evidence of neuroprotection - Choline
a. Overview of biologic roles
b. Dietary intakes, implications for meeting bodily requirements
c. Mechanisms of neuroprotection
d. Research evidence supporting citicoline for attention, memory
e. Magnesium and citicoline - Carnitine
a. Overview of biologic role, significance
b. Effects on mitochondrial function, metabolism
c. Proposed neuroprotective mechanisms
d. Research supporting utility for neurocognitive disorders - Psychosocial Factors: Loneliness
a. A new era: COVID19
b. Cognitive and affective sequelae of prolonged loneliness, isolation
c. Loneliness and dementia: the research - Recapping the Functional Medicine Approach
a. Targeted interventions
b. Diet
c. Essential testing
d. Illuminating the THE ZEEBRA model
e. The shifts towards proactive medicine
- Oligomeric Proanthocyanidins (OPCs)
All refunds must be requested within seven (7) days of enrollment. In order to qualify for a refund, learners must have progressed through less than 10% of the educational content in question. All refunds will be processed minus a 10% transaction fee.
A Glimpse Into Alzheimer’s Disease
The global burden of Alzheimer’s Disease, neurodegenerative disorders, and cognitive decline is massive. Every 65 seconds, someone is diagnosed with Alzheimer’s Disease; it is the 6th leading cause of death nationwide, and the only one amongst the top ten for which there is no cure. Despite extensive research, traditional medicine and treatments have come up short from curing this terrible disease. Attempts to find a viable pharmaceutical cure have, thus far, failed, and the tolls borne by victims and family members alike remain incalculable.
Research has confirmed Alzheimer’s to have a substantial prodrome; the biologic processes underlying progressive cognitive decline may in fact commence decades before symptoms begin to manifest. The discovery of a lengthy prodrome in Alzheimer’s and other dementias is cause for hope. A prodrome represents a window of opportunity, a chance to steer neurologic aging towards health, and to modify certain etiologic factors while they remain modifiable. Such factors are tools that can be wielded to potentially significant effect in a functional medicine model centered upon prevention.
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