Alzheimer’s Disease

According to current statistics, 1 in every 10 of us reading this article will have Alzheimer’s dementia by the time we are 65 years old. That risk will double every 5 years of our lives. Other sobering statistics from the Alzheimer’s Association reveal that 1 in 3 seniors die with Alzheimer’s or another dementia, and it kills more than breast cancer or prostate cancer combined….. At the American Academy of Optometry’s Spring 2018 meeting in San Antonio, Dr. George Perry, dean of the College of Sciences and the Semmes Foundation Distinguished Chair in Neurobiology at The University of Texas at San Antonio, gave an intriguing lecture on Alzheimer’s disease during the Nutrition, Disease, Prevention, & Wellness SIG Symposium. Dr. Perry is distinguished as one of the top 10 Alzheimer's disease researchers with over 1,000 publications, and he is one of the top 100 most-cited scientists in Neuroscience & Behavior. Perry serves as editor-in-chief for the Journal of Alzheimer's Disease and he is the President for the American Association of Neuropathologists. Dr. Perry is a renegade in Alzheimer’s research. Elucidating oxidative damage as the initial cytopathological abnormality in Alzheimer’s disease, he eschews the amyloid cascade hypothesis, long considered dogma, that has driven Alzheimer’s research since 1992. The belief that deposition of amyloid β protein, the main component of the plaques in Alzheimer’s brains, is the causative agent of Alzheimer’s pathology and that the neurofibrillary tangles, cell loss, vascular damage, and dementia follow as a direct result of this deposition have led hundreds of scientists in academia and industry (at a cost of tens of billions of dollars) down the wrong path, according to Dr. Perry. He believes that there is a relationship, but not a causal one. Plaques, he said, may be a byproduct of biological processes aimed at protecting the brain. After 30 years and $24 billion invested in efforts to reduce plaques (that have not resulted in any effective treatments for the disease), Perry’s hypothesis is considered controversial but it is gaining traction. See the article below:

Is Alzheimer's Research On the Wrong Track?

Emerging science suggests that, instead of acting as villains, amyloids may actually function as molecular guardians dispatched to silence inflammation and mop up errant cells after an injury
as part of the body’s waste management system. “The presence of amyloids is a protective response to something going wrong, a threat,” says Dr. Dale Bredesen, a UCLA neurologist. “But the problem arises when the threats are chronic, multiple, unrelenting and intense. The defenses the brain mounts are also intense and these protective mechanisms cross the line into causing harm, and killing the very synapses and brain cells the amyloid was called up to protect.”

During Dr. Perry’s lecture at the academy, he recommended a new book published by the UCLA neurologist Dr. Dale Bredesen, The End Of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline. In his book, Dr. Bredesen discusses research that challenges the central dogma of Alzheimer’s and shows that this devastating disease is the result of a normal, healthy brain process that has gone haywire. That is, the brain suffers some injury, infection, or other assault and responds by defending itself. The defense mechanism includes producing the Alzheimer’s-associated amyloid. Yes, you read that correctly—the amyloid that has been vilified for decades, the very amyloid that everyone has been trying to get rid of, is part of a protective response, according to the research that he highlights. Contrary to the current dogma, therefore, what is referred to as Alzheimer’s disease in his view is actually a protective response to, specifically, three different processes “inflammation, suboptimal levels of nutrients and other synapse-supporting molecules, and toxic exposures.” Dr. Bredesen states in his book “the realization that Alzheimer’s disease can exist in three distinct subtypes (and often in combinations of these subtypes) has profound implications for the way we evaluate, prevent, and treat it. That discovery also means that we can better treat the subtler forms of cognitive loss, mild cognitive impairment and subjective cognitive impairment, before they progress to full-blown Alzheimer’s disease.” Dr. Bredesen‘s studies are worth reading and his protocol, which although is intensive and broken down into addressing the three subtypes he mentions, offers steps that can be taken to change the path of the devastating effects of cognitive decline, which starts as early as your 40’s. This book is especially important for those who carry the ApoE4 gene, which is the strongest known genetic risk factor for Alzheimer’s disease. Carrying one ApoE4 (that is, inherited from one parent) increases your lifetime risk of Alzheimer’s to 30 percent, while carrying two copies (inheriting copies from both parents) increases it to well over 50 percent (from 50 to 90 percent, depending on which study you read). That compares to a risk of only about 9 percent in people who carry zero copies of this allele. Dr. Bredesen posits that this group could benefit the most by his protocol, as genes aren’t always destiny and risk can be mitigated through lifestyle and epigenetics. Changes made early, before symptoms arise, can mean the difference between a very grim future verses one of thriving. Hence, REPAIR THE ROOF BEFORE IT STARTS RAINING.

Our president emeritus, Dr. Stuart Richer, has been studying the potential role we have in detecting Alzheimer’s disease for years. In fact, the first patient Dr. Bredesen references in his book, patient zero, found out about the presence of her amyloid by a retinal scan. In the article below, Dr. Richer states the following: “The eye and brain share similar embryologic origins,” noting that Alzheimer’s affects visual fields, eye movements, and pupil and optic nerve function, as well as the brain “As ODs, we intimately examine the ocular-cerebral system daily Noninvasive imaging techniques have emerged that accurately and noninvasively detect and monitor amyloid deposition in the human lens and retina. For AD cataracts, a commercial device involving a fluorescent amyloid ligand eye drop and slit-lamp based detection system, has undergone clinical trials. AD Retinal imaging technology is also close at hand.” Please see his article below:

Dr. Richer referred me to this article recently published on April 2, 2019 titled “Parafoveal vessel loss and correlation between peripapillary vessel density and cognitive performance in amnestic mild cognitive impairment and early Alzheimer’s Disease on optical coherence tomography angiography” click on the link below.

The study concludes: “OCTA shows significant decline in parafoveal flow and VD in individuals with early cognitive impairment related to AD, suggesting that these parameters could have potential utility as early disease biomarkers. In contrast, the presence of larger vascular channels in the peripapillary region may have obscured subtle capillary changes in that region. Overall, the correlation between vascular OCTA parameters and cognitive performance supports further OCTA studies in this population.”

In Conclusion:
When I heard Dr. Perry recommend Dr. Bredesen‘s book at his lecture at the Academy, I took note of it and texted the name and reference to a friend of mine who may likely carry the ApoE4 gene allele. Her father, a Columbia University law graduate and judge in New York, was diagnosed with early onset Alzheimer’s in his 50’s and passed away from the disease. I then forgot about the book, until recently, when I was listening to a lecture by the New York Times best selling author and neurologist, Dr. David Perlmutter, who referenced the book and called Dr. Bredesen‘s work “Nobel prize worthy”. With a moderate degree of skepticism, I bought the book and began reading it on a flight, and once I began reading it I could not put it down. The basic tenets of the book, healing the brain and addressing oxidative stress, are essentially what healed my son’s brain from the ravages of neuroinflammation and autism 15 years ago.

Although writing about science requires a dispassionate tone devoid of personal stories, I thank you for allowing me this chance to share the source of my passion for nutritional medicine and
lifestyle interventions, my son’s journey of healing and now thriving.

Please give a reference to Lisa Renzi’s Ted Talk for our members.

Please also mention Dorothy being honored in Women in Optometry…Great pickup!!!