The Eye As A Window to Alzheimer’s Disease

I had the pleasure of attending an incredible lecture yesterday at the AOA meeting in Boston, presented by Peter J. Snyder, Ph.D.


As Dr. Snyder pointed out, he’s not the fist one to consider that the eye may provide earlier biomarkers for Alzheimer’s Disease.  At least thirteen years ago, researchers were suggesting correlations between beta amyloid deposition in the crystalline lens and AD.  Nine years ago an article was published in IOVS looking at hemodynamic parameters and RNFL (Retinal Nerve Fiber Layer) loss in early AD.  In fact, as I was touring the exhibit hall, I came across a new book from Springer which contained a chapter on OCT in Alzheimer’s disease.


Dr. Snyder reinforced the urgency of earlier identification of Alzheimer’s due to the rapidity with which baby boomers are approaching prime time for the disease.


Preclinical AD is a term that originated in 2011.  It is an early stage during which cognitive changes are subtle and hard to measure with precision.  In fact the best indication, particularly when a person is bright, comes from increasing self-awareness of senior moments.  In a way this was reminiscent of how we think of gifted children with learning problems.  It is often the self-awareness that one is struggling more than one’s peers that indicates that if clinical tests are negative, we haven’t found the right test.  Although Preclinical AD is the stage in which the disorder is hardest to identify, but also the disease stage for which neuroprotective therapies might prove to be most effective.


But Dr. Snyder suggested that the presence of inclusion bodies in the IPL (Inner Plexiform Layer) may prove to be the earliest biomarker at the retinal level.  This is because the CNS beta amyloid burden reveals itself in inflammation that differentially thickens the IPL more so than other retinal layers.


Ultimately larger scale studies will be necessary, and pinpointing which technologies will be most reliable in revealing retinal inclusion bodies indicative of beta amyolid accumulation is crucial.  None of this should be all that surprising to developmental optometrists, because we have been touting the significance of the retina as brain tissue for many years.  It is exciting now to unify issues in development with issues in neuroprotection that might allow for more effective early intervention in later stages of life.

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