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Hope for Patients With Alzheimer’s


Not only does Alzheimer’s disease (AD) contribute to high mortality rates in the elderly,1 it also places an enormous burden on families and the healthcare system.2 As the world population continues to age,3 the cumulative growth of patients with AD and the high levels of comorbidities present in these patients4,5 present an increasing challenge for clinicians.

There are many known AD risk factors, including vascular and metabolic health, diabetes, smoking, obesity, stroke, depression, and traumatic brain injury.6 As the leading cause of dementia, AD is an especially crucial arena for both preventative interventions and lifestyle modifications that can slow the course of the disease.

Functional Medicine is especially well equipped to minimize these risk factors. In addition, many of the lifestyle factors that seem to protect against the development of AD are common tools for Functional Medicine practitioners, including a nutrient-rich diet,6 7,9 physical activity,6,7 and intellectual and psychosocial engagement and support.6,8 In addition, we know that Alzheimer’s and cognitive decline have many different causes, including vascular dysfunction and toxic exposure. It is possible to stratify patients with AD and cognitive decline by cause and focus on the appropriate treatments for that cause. The clinical subtypes and specific multimodal treatments for each clinical subtype will be detailed at Reversing Cognitive Decline.

Join IFM and MPI Cognition for an Advanced Clinical Training (ACT) on preventing, slowing, and even reversing dementia and AD. You will learn to personalize and treat patients to reduce their risks, improve their vitality, and decrease associated health risks.

  1. James BD, Leurgans SE, Hebert LE, Scherr PA, Yaffe K, Bennett DA. Contribution of Alzheimer disease to mortality in the United States. Neurology. 2014;82(12):1045-50. doi: 10.1212/WNL.0000000000000240.
  2. PBS. Alzheimer’s: Every Minute Counts. [video] St. Paul, MN. TPT National Productions; 2017. http://www.pbs.org/video/2365941501/. Aired January 25, 2017. Accessed February 8, 2017.
  3. He W, Goodkind D, Kowal P. An aging world: 2015. International population reports. United States Census Bureau. https://www.census.gov/content/dam/Census/library/publications/2016/demo/p95-16-1.pdf. Published March 2016. Accessed February 8, 2017.
  4. Santos García D, Suárez Castro E, Expósito I, et al. Comorbid conditions associated with Parkinson's disease: a longitudinal and comparative study with Alzheimer disease and control subjects. J Neurol Sci. 2017 Feb;373:210-15. doi: 10.1016/j.jns.2016.12.046.
  5. Clague F, Mercer SW, McLean G, Reynish E, Guthrie B. Comorbidity and polypharmacy in people with dementia: insights from a large, population-based cross-sectional analysis of primary care data. Age Ageing. 2017;46(1):33-39. doi: 10.1093/ageing/afw176.
  6. Reitz C, Brayne C, Mayeux R. Epidemiology of Alzheimer disease. Nat Rev Neurol. 2011;7(3):137-52. doi: 10.1038/nrneurol.2011.2.
  7. Scarmeas N, Luchsinger JA, Schupf N, et al. Physical activity, diet, and risk of Alzheimer disease. JAMA. 2009;302(6):627-37. doi: 10.1001/jama.2009.1144.
  8. Monsell SE, Mock C, Roe CM, et al. Comparison of symptomatic and asymptomatic persons with Alzheimer disease neuropathology. Neurology. 2013;80(23):2121-29. doi: 10.1212/WNL.0b013e318295d7a1.
  9. Gu Y, Nieves JW, Stern Y, Luchsinger JA, Scarmeas N. Food combination and Alzheimer disease risk: a protective diet. Arch Neurol. 2010;67(6):699-706. doi: 10.1001/archneurol.2010.84.

Strategies to Assess and Subtype Cognitive Decline Patients

The recent discovery that there appears to be different subtypes of Alzheimer’s disease (AD) should come as little surprise: much of what we lump together under the banner of a particular disease is actually a collection of very distinct etiologies (e.g., “cancer”). Equally unsurprising, then, should be the finding that different treatments are required to address the various subtypes.


For example, Dale Bredesen, MD, has identified an Alzheimer’s subtype associated with toxic exposures.1 This subtype, labeled type 3 or cortical Alzheimer’s, typically develops early, when patients are in their late 40s to early 60s.1,2 It usually appears after anesthesia, menopause, andropause, or a period of extreme stress or sleep loss.2 Instead of having problems forming short-term memories, type 3 patients have problems maintaining long-term memories. These problems include difficulty calculating or finding the right words.2 They also have poor executive function and are often depressed or passive.1,2 And lab tests frequently show low levels of zinc or high ratios of copper to zinc.1

Learn about all the known subtypes of AD and effective strategies for preventing and even reversing each in the early stages at IFM’s new program, Reversing Cognitive Decline: Advanced Clinical Training in Treating MCI and Early Alzheimer’s Disease. Clinicians will learn:

  • Optimal assessment strategies for patients with MCI and early AD.
  • A new way to stratify patients into specific subtypes based on the likely causes of their dysfunction.
  • Multimodal protocols to individualize treatments for each patient that address the appropriate underlying causes.

Join IFM, in collaboration with Dale Bredesen, MD, and MPI Cognition, and learn a new approach to the treatment of early stage AD and MCI that has already proven to be remarkably effective in arresting cognitive decline and in many cases even reversing it. Limited seating is available at this program, so register today.

  1. Bredesen DE. Inhalational Alzheimer’s disease: an unrecognized — and treatable — epidemic. Aging (Albany NY). 2016;8(2):304–13. doi: 10.18632/aging.100896.
  2. Bredesen DE. Metabolic profiling distinguishes three subtypes of Alzheimer’s disease. Aging (Albany NY). 2015;7(8):595–600. doi: 10.18632/aging.100801.

Therapies to Restore and Maintain Healthy Cognition

Dale Bredesen, MD

America’s population is aging, and cognitive decline is a major concern for many older patients. Patients seek strategies to prevent and maintain their cognitive faculties, even in the face of normal, age-related cognitive decline.1

Dale Bredesen, MD, is one of the researchers whose multimodal approach has yielded successful outcomes addressing the pathogenesis of Alzheimer’s disease (AD) through personalized dietary and lifestyle intervention. In one small case study, personalized treatment improved cognition over a period of 3–6 months in 90% of patients with AD or its precursors.2 In another similar study, most neuropsychological results improved when patients were treated with a personalized protocol for 5–24 months.3 In both studies, patients were able to resume employment or improve their job performance.

IFM is collaborating with MPI Cognition and Dr. Bredesen to present a two-day CME on Reversing Cognitive Decline. The course focuses on translating current research findings into effective therapies for AD and its precursors, mild or subjective cognitive impairment.

Learn from expert educators, including Dr. Bredesen, who will address current, in-depth research about reversing neurodegeneration this March 11-12, in Huntington Beach, CA. Become an expert at Reversing Cognitive Decline by differentiating and addressing mild cognitive impairment and the six subtypes of Alzheimer’s disease.

  1. Harada CN, Natelson Love MC, Triebel K. Normal cognitive aging. Clin Geriatr Med. 2013;29(4):737-52. doi: 10.1016/j.cger.2013.07.002.
  2. Bredesen DE. Reversal of cognitive decline: a novel therapeutic program. Aging. 2014;6(9):707-17. doi: 10.18632/aging.100690.
  3. Bredesen DE, Amos EC, Canick J, et al. Reversal of cognitive decline in Alzheimer’s disease. Aging. 2016;8(6):1250-58. doi: 10.18632/aging.100981.

Differentiate the Six Major Subgroups of Alzheimer’s Disease

Is there an environmental form of Alzheimer’s with treatable causes? According to Dale Bredesen, MD, type 3 Alzheimer’s disease (AD) is the result of exposure to specific toxins.1 For example, type 3 AD is associated with exposure to toxic mold in water-damaged buildings as well as toxic levels of copper and mercury.1

blue neurons

The onset of type 3 AD skews younger, developing in patients in their 40s to 60s.1,2 It typically appears following anesthesia, menopause, andropause, or a period of extreme stress or sleep loss.2 Furthermore, patients with type 3 AD have problems maintaining long-term memories, which results in dyscalculia and aphasia.2

These and other unique features of type 3 AD indicate that it “may be mediated by a fundamentally different pathophysiological process” compared to the other five subtypes of AD, as Bredesen has noted.1 In this way, treatment of type 3 AD may also differ from other subtypes. For instance, while anti-amyloid therapy seems to be effective for other subtypes, it could worsen the condition of patients with type 3 AD because amyloid helps protect patients from the effects of toxins.1 Instead, patients with type 3 AD benefit more from identifying and removing the specific toxins responsible for their cognitive decline.1

IFM’s inaugural Advanced Clinical Training (ACT), taking place March 11-12, 2017, will address a systems-biology approach to Reversing Cognitive Decline. Learn from Dr. Bredesen and other experts about the many underlying factors that may lead to all six major subtypes of AD, including air pollution3,4 and vascular health.5,6,7 Improve your diagnostic skills in recognizing the six subtypes of AD, in addition to mild cognitive impairment (MCI), to arrest cognitive decline and in many cases even reverse it.


Special Offer! IFM's 2017 Annual International Conference (AIC), on the topic of neuroplasticity, is the perfect complement to the clinical content to be presented in March. Register to attend both to receive:

  • $300 off Reversing Cognitive Decline
  • $100 off AIC (early bird discount)
to attend AIC & Reversing Cognitive Decline

Can't attend both conferences?

to attend Reversing Cognitive Decline only

  1. Bredesen DE. Inhalational Alzheimer’s disease: an unrecognized—and treatable—epidemic. Aging. 2016;8(2):304-13. doi: 10.18632/aging.100896.
  2. Bredesen DE. Metabolic profiling distinguishes three subtypes of Alzheimer’s disease. Aging. 2015;7(8):595-600. doi: 10.18632/aging.100801.
  3. Calderón-Garcidueñas L, Leray E, Heydarpour P, Torres-Jardón R, Reis J. Air pollution, a rising environmental risk factor for cognition, neuroinflammation and neurodegeneration: the clinical impact on children and beyond. Rev Neurol. 2016;172(1):69-80. doi: 10.1016/j.neurol.2015.10.008.
  4. Oudin A, Forsberg B, Adolfsson AN, et al. Traffic-related air pollution and dementia incidence in northern Sweden: a longitudinal study. Environ Health Perspect. 2016;124(3):306-12. doi: 10.1289/ehp.1408322.
  5. Musicco M, Palmer K, Salamone G, et al. Predictors of progression of cognitive decline in Alzheimer’s disease: the role of vascular and sociodemographic factors. J Neurol. 2009;256(8):1288-95. doi: 10.1007/s00415-009-5116-4.
  6. Wang M, Norman JE, Srinivasan VJ, Rutledge JC. Metabolic, inflammatory, and microvascular determinants of white matter disease and cognitive decline. Am J Neurodegener Dis. 2016;5(5):171-77.
  7. Gorelick PB, Scuteri A, Black SE, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(9):2672-713. doi: 10.1161/STR.0b013e3182299496.

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