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Default Dr. Dale Bredesen on Preventing and Reversing Alzheimer's Disease

Dr. Dale Bredesen on Preventing and Reversing Alzheimer's Disease 10-1-2018 Dr. Rhonda Patrick

Dr. Dale Bredesen on Preventing and Reversing Alzheimer's Disease < video

Dale E. Bredesen, M.D., is a professor of neurology at the Easton Laboratories for Neurodegenerative Disease Research at the David Geffen School of Medicine at the University of California, Los Angeles (UCLA).

Dr. Bredesen’s laboratory focuses on identifying and understanding basic mechanisms underlying the neurodegenerative process and the translation of this knowledge into effective treatments for Alzheimer’s disease and other neurodegenerative conditions. He has collaborated on the publication of more than 220 academic research papers.

He and his colleagues have identified several subtypes of Alzheimer’s disease and has developed ReCODE – reversal of cognitive decline – a protocol that offers a new approach to treatment that has reversed symptoms in patients with mild cognitive impairment and Alzheimer’s disease.

Dr. Bredesen received his undergraduate degree from the California Institute of Technology and his medical degree from Duke University. He served as Resident and Chief Resident in Neurology at the University of California, San Francisco (UCSF). He was the Founding President and CEO of the Buck Institute for Research on Aging and Adjunct Professor at UCSF.
The major subtypes of Alzheimer’s disease.

Identified just over a century ago, Alzheimer’s disease is a complex, multifaceted condition that affects nearly 44 million people worldwide. In this episode, Dr. Dale Bredesen identifies the defining characteristics of Alzheimer’s disease and enumerates its primary subtypes:

The inflammatory subtype of Alzheimer’s disease.
A type characterized by systemic inflammation, reflected in such laboratory results as a high hs-CRP (high-sensitivity C-reactive protein), low albumin:globulin ratio, and high cytokine levels such as interleukin-1 and interleukin-6.
The atrophic subtype of Alzheimer's disease — a reduction in support for synaptogenesis.
A type characterized by an atrophic profile, with reduced support from molecules such as estradiol, progesterone, brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), testosterone, insulin, and vitamin D, often accompanied by increased homocysteine and insulin resistance, the last feature of which Dr. Bredesen refers to as type 1.5 or glycotoxicity.
The cortical subtype of Alzheimer's disease — an environmental toxin-related type associated with chronic Inflammatory response syndrome (CIRS) that presents with more general cerebral atrophy and frontal-temporal-parietal abnormalities, resulting in an emphasis on executive deficits, rather than the more amnestic quality of hippocampal impairment.

Although the subtypes vary in their causes and manifestation and often overlap to some degree, Dr. Bredesen explains that the underlying pathological features – the accumulation of amyloid beta plaques and tau tangles – are unifying aspects of the disease. He adds that how these features play out in the somewhat fragile environment of the brain depends on a wide array of contextual parameters, such as genetics and lifestyle factors, including diet, sleep, exercise, and environmental exposures.
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