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    ODs’ role promising in detecting Alzheimer’s disease

    Examining ocular-cerebral system daily may help ODs detect amyloids early

    More than 5 million Americans, 70 percent of all dementia patients, and their loved ones are currently living with Alzheimer’s disease (AD), and that number is expected to rise to 16 million by 2050.1

    There are two principal forms of Alzheimer’s disease:

    • Early-onset primarily genetically-based disease accounting for only approximately 1 percent of all cases

    • Late-onset primarily environmentally-influenced Alzheimer’s disease associated with the apo-E4 gene and generally starting after age 60.2

    Previously from Dr. Richer: How zinc affects AMD

    In early-onset AD, hundreds of mutations have been identified in three different genes. All mutations affect the metabolism of a sticky and aggregating short peptide known as the amyloid ß-protein.3

    The eye-brain nexus

    The eye and brain share similar embryologic origins. AD also affects visual fields, eye movements, and pupil and optic nerve function.4 As ODs, we intimately examine the ocular-cerebral system daily.  There is an intimate connection between amyloid ß-protein found in AMD drusen, a type of peripheral cortical cataract, and AD pathology.5,6

    Noninvasive imaging techniques have emerged that accurately and noninvasively detect and monitor amyloid deposition in the human lens and retina.4 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.8

    Related: OD education must keep up with industry changes

    Amyloid ß-protein

    The causes of late-onset AD are not well understood, and patients can develop amyloid plaques with or without succumbing to AD. More than 250 clinical trials have been conducted on a variety of amyloid cascade treatments—including several that can remove amyloid ß-protein from the brain. All have failed to halt AD progression.2,9,10

    Amyloid ß-protein is a marker of AD but is not sufficient in itself to develop AD. Other biochemical and morphological features of AD. These features include altered calcium, phospholipid, cholesterol, and sugar metabolism, as well as mitochondrial dynamics and function that appear prior to plaque (amyloid) and tangle (τ protein) accumulation.10

    As ODs, we examine about one-third of the U.S. population yearly. Whether you are scientifically inclined to be an “amyloidist” or “tauist” (τ protein), the clinical imperative is eliminating these oculo-cerebral toxins. This is accomplished by counseling patients on how to reduce environmental toxins such as sugar and prescribing nutrients for repair and maintenance of both the eyes and brain.

    Stuart Richer, OD, PhD, FAAO
    Stuart Richer, OD, PhD, FAAO, is director of ocular preventive medicine at James Lovell Federal Health Care Facility in Chicago. He is ...


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