The Official Website for The Nemechek Protocol™ Medical Recovery Program

CASE REPORT: Remission of Alzheimer’s Disease with tVNS in Combination with an Anti-Neuroinflammatory Regimen


Traumatic brain injuries lead to microdamage in the brain triggering an injury repair response.

The response consists of a neuroinflammatory and regeneration phases involving microglia, neurotrophins and neurogenesis (See figure 1).1,2

Severe TBI increase the risk of Alzheimer’s Disease (AD) 4-fold whereas individuals with moderate TBI were twice as likely to have AD in late life compared with controls.3

Pro-inflammatory cytokines also contribute to the progressive nature of Alzheimer’s Disease as well as impair the neuronal repair process (See figure 2). One source producing these cytokines are primed M1-microglia.4

Diffuse M1-microglia infiltration throughout multiple brain regions in person’s suffering from Alzheimer’s dementia in post-mortem studies.5

Figure 1: Neuron Repair Process

Figure 2 Neuroinflamation and Dysfunction of Neuron Repair Process

We theorized that shifting microglia to the anti-inflammatory rejuvenating M2-phenotype and reducing pro-inflammatory cytokines levels would improve the brain’s injury repair response sufficiently to alter the natural course of AD.

The Nemechek Protocol utilizes transcutaneous vagus nerve stimulation (tVNS) 6,7 high concentration docosahexaenoic acid (DHA) fish oil 8, 9, olive oil 10, curcumin11, acetyl-l-carnitine and 10-day course of rifaximin12 to achieve these goals.

Vagus nerve stimulation has been previously tested with some success in older adults with memory problems and AD but not in combination with a multi-faceted anti-inflammatory.13, 14

We are excited to report the clinical remission of 2 individuals with advanced AD using such an approach. While another group has reported remissions of AD, we are the first to present 2 cases of rapid Alzheimer’s remission with the use of tVNS.15


The subjects were two men (age: subject #1 – 62, subject #2 – 67) who had been diagnosed with Alzheimer’s Disease by their neurologist. Secondary consultation with neurologists confirmed the diagnosis of Alzheimer’s.

Subject #1 was a financial planner had been experiencing increasing cognitive issues for 2-3 years. He was having difficulty with mathematical computations and was forced into disability. At the time of enrollment, Subject #1 would forget what he was going to say in approximately 50% of all his sentences. It was necessary for his daughter to provide all medical background as well as transportation.

Subject #2 was a general contractor and business owner who had been experiencing progressive inability to operate his business. For the prior 18 months, he was unable to manage his construction company he had run for 30 years. At the time of enrollment, Subject #2 was completely incapable of communicating any aspect of his medical history, and required his wife to provide all information as well as transportation.

Both subjects were started on the Nemechek Protocol, a regimen designed to normalize brain recovery mechanisms though shifting of microglia to the M2-phenotypes and suppression of systemic pro-inflammatory cytokines.

The protocol consists of:

  • tVNS (5 Hz, 250 uS, 1 mA, continuous), 2 hours (cumulative time on device), patient-administered via the tragus or concha)
  • Rifaximin, 550 mg BID x 10 days
  • Fish Oil containing 3,000 mg of DHA and 1,500 mg of EPA
  • Curcumin 1,000 mg twice daily
  • Acetyl-l-Carnitine 1,000 mg twice daily

Clinical and Autonomic Monitoring Every 2-3 Months:

  • Cognition improvement was based on clinical assessment
  • Autonomic assessment was performed via spectral analysis (ANSAR Inc., ANX 3.0)


After 10 and 7 months of treatment, both subjects experienced complete resolution dementia symptoms as well as improvement of their resting autonomic indices.


“Dramatic recovery of cognitive function and independence within 10 months of treatment.”



  • MMSE = 24
  • Patient is unable to communicate his medical history because of speech and cognition issues.
  • 75% of all attempts to speak fail because he cannot complete sentences; loses his train of thought.
  • Also with lightheadedness, balance issues, anxiety, chronic depression.
  • Requires family member for transportation and to provide history.


  • Speech is noticeably clearer and more fluid.
  • Friends and family comment on his improvement.
  • Lightheadedness, and anxiety are improved.


  • Marked improvement in speech.
  • Able to converse about recent events without difficulty.
  • Loses track of only 5 sentences during a 60-minute medical encounter.
  • No family member required to assist in plane travel or medical encounter.


  • MMSE = 28
  • Does not lose track of a single sentence during a 60-minute medical encounter.
  • Insomnia, and anxiety are greatly improved.
  • Balance is improving but still with occasional lightheaded sensation.






“Clinical remission of Alzheimer’s Disease within 5 months of therapy with tVNS.”



  • Patient is unable to communicate his medical history because of memory and general cognition issues.
  • Cognition does not improve with exercise or laying supine.
  • Requires family member for transportation and to provide medical history.


  • Sleep, energy and headaches are still greatly improved.
  • His cognitive interaction during examination is noticeably improved.


  • Marked improvement in cognition.
  • Has returned to work and managing contractor at work.
  • No family member required to drive to the office nor assist in medical encounter.


  • Marked improvement in cognition.
  • Has returned to work as managing contractor.
  • Can safely drive himself to work and office visits.






tVNS in combination with an anti-inflammation suppressive regimen, dramatically restored cognitive function in 2 subjects with moderately advanced Alzheimer’s dementia within 5 months. (See figure3)

Obvious subjective improvement, was noted by the patient, their significant other, and their family members. After 5 months, they sustained complete clinical recovery of Alzheimer’s dementia.

The ability of tVNS to reverse dementia may be though its ability to suppress inflammatory, alteration of microglia phenotype and induce neuroplasticity.

Without tVNS, the same regimen was incapable of reversing Alzheimer’s dementia is 3 prior patients.

Interestingly, continuous rather than cyclical VNS improves cognitive function. Our prior work utilizing tVNS in autonomic dysfunction suggested a 2-hour minimum daily stimulation was required to clinically and objectively benefit the patients.

We theorize that longer continuous tVNS may be more effective at the induction of neuroplasticity than cyclical stimulation.


By the year 2030 76 million people are estimated to be living with Alzheimer’s Disease globally.

The simplicity and low cost of this treatment regimen could have enormous global impact if this effect is shown to be effective in larger clinical trials.

Smaller, vagus stimulators could comfortably be worn by individuals in the earliest stages of the disease.


1. Wager-Smith, Karen, and Athina Markou. “Depression: A Repair Response to Stress-Induced Neuronal Microdamage That Can Grade into a Chronic Neuroinflammatory Condition?” Neuroscience and biobehavioral reviews 35.3 (2011): 742–764.

2. Sun, Rao et al. “Hippocampal Activation of Microglia May Underlie the Shared Neurobiology of Comorbid Posttraumatic Stress Disorder and Chronic Pain.” Molecular Pain 12 (2016): 1744806916679166.

3. Plassman BL, Havlik RJ, Steffens DC, Helms MJ, Newman TN, Drosdick D, et al. “Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias.” Neurology. 2000; 55:1158–66.

4. McKee A and Robinson M. “Military-related traumatic brain injury and neurodegeneration.” Alzheimers Dement. 2014 June; 10(3 0): S242–S253.

5. Gomez-Nicola, Diego, and Delphine Boche. “Post-Mortem Analysis of Neuroinflammatory Changes in Human Alzheimer’s Disease.” Alzheimer’s Research & Therapy 7.1 (2015): 42.

6. Zhang Q et al. “Activation of the α7 nicotinic receptor promotes lipopolysaccharide-induced conversion of M1 microglia to M2.” Am J Transl Res 2017;9(3):971-985.

7. Meneses, G. et al. “Electric Stimulation of the Vagus Nerve Reduced Mouse Neuroinflammation Induced by Lipopolysaccharide.” Journal of Inflammation (London,
England) 13 (2016): 33.

8. Chang, Philip K-Y et al. “Docosahexaenoic Acid (DHA): A Modulator of Microglia Activity and Dendritic Spine Morphology.” Journal of Neuroinflammation 12 (2015): 34.

9. Harvey, Lloyd D. et al. “Administration of DHA Reduces Endoplasmic Reticulum Stress-Associated Inflammation and Alters Microglial or Macrophage Activation in Traumatic Brain Injury.” ASN NEURO 7.6 (2015): 1759091415618969.

10. Liu, Joanne J. et al. “Pathways of Polyunsaturated Fatty Acid Utilization: Implications for Brain Function in Neuropsychiatric Health and Disease.” Brain research (2015): 220–246.

11. Petraglia, Anthony L., Ethan A. Winkler, and Julian E. Bailes. “Stuck at the Bench: Potential Natural Neuroprotective Compounds for Concussion.” Surgical Neurology International 2 (2011): 146.

12. Gao J et al. “Rifaximin, gut microbes and mucosal inflammation: unraveling a complex relationship.” Gut Microbes. 2014 Jul 1;5(4):571-5.

13. Jacobs HI et al. “Transcutaneous vagus nerve stimulation boosts associative memory in older individuals.” Neurobiol Aging. 2015 May;36(5):1860-7.

14. Merrill CA et al. “Vagus nerve stimulation in patients with Alzheimer’s disease: Additional follow-up results of a pilot study through 1 year.” J Clin Psychiatry. 2006 Aug;67(8):1171-8.

15. Bredesen, Dale E. et al. “Reversal of Cognitive Decline in Alzheimer’s Disease.” Aging (Albany NY) 8.6 (2016): 1250–1258.

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