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A Systems-Biology Approach to Reversing Cognitive Decline

A Systems-Biology Approach to Reversing Cognitive Decline
Dale Bredesen, MD

Is there an environmental form of Alzheimer’s with treatable causes? According to researcher 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

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 differentiate it from the other five subtypes of AD, as Bredesen has noted.1 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 formerly offered the Reversing Cognitive Decline Advanced Clinical Training. Dr. Bredesen and other experts spoke 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

Explore Other Ways to Support Patients with Cognitive Decline

References

  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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