Are Your Eyes the Key to Predicting Alzheimer’s?

A recent breakthrough in the fight against Alzheimer’s disease suggests that beta amyloid protein in the retina of the eye corresponds directly to the same amount of protein in the brain.Are Your Eyes the Key to Predicting Alzheimer's?

Learn more about how your eyes could be the key to predicting Alzheimer’s.

Predicting Alzheimer’s

We don’t have a crystal ball that tells us our future. But when it comes to whether or not we’re going to develop Alzheimer’s, there is a new test that just might give us a serious glimpse into our fate.

Researchers at Cedars-Sinai Medical Center in Los Angeles discovered that beta amyloid protein, a dementia-causing protein in the brain, can also be found in the retina of the eye; giving the medical community a much simpler way to predict the disease.

This is great news, considering Alzheimer’s disease is expected to rise from 5.1 million in 2010 to 13.5 million in 2050 and is the only cause of death among the top 10 in the U.S. that cannot be prevented, cured or even slowed, according to the Alzheimer’s Association.

Since Alzheimer’s disease begins its destructive path in the brain 10-20 years before there are any symptoms — and by the time symptoms do show, brain cells have been destroyed by as much as 40-50% — this research helps with not only early diagnosis, but also Alzheimer’s clinical trials and prevention efforts. But, unfortunately, there’s still a lot of work to be done.

Would You Want to Know Your Future Even if You Couldn’t Change it?

Last year, the FDA approved an Alzheimer’s brain amyloid imaging PET scan that “could potentially be helpful in the diagnosis of people with cognitive impairment when considered along with other clinical information, and when performed according to standardized protocols by trained staff.”

But the scan is both invasive and not entirely definitive. Furthermore, it can be hard to say who the ideal candidate would be for such a procedure.

Perhaps the biggest risk factor is psychological, though. While candidates might be able to see into their future, Alzheimer’s has no known cure. Living with this knowledge could have negative consequences on a person’s psyche.

What’s in the Eyes of the Beholder

Now there’s something newer and simpler to find the disease. A retinal test that can detect these same brain amyloid plaques, a known marker for the disease. Some neurologists suspect the test can indicate markers 10 years out while others say it’s as much as 20 years ahead.

According to Primary Care Optometry News, “Neurologists have theorized a correlation between the amount of amyloid in the eye and amyloid in the brain. If correct, the retina could be the solution to early detection and treatment of Alzheimer’s disease (AD), as amyloid beta protein accumulation may begin approximately 20 years prior to memory loss symptoms.”

So let’s say you – or your loved one – decides to get this test. What then?

“Most people, if they’re going to get AD, start developing the pathology hallmarks, such as amyloid deposits, in their 50s,” Keith L. Black, MD, chairman and professor of the Department of Neurosurgery at Cedars-Sinai Medical Center in Los Angeles, and cofounder of NeuroVision, said. “The key for having an effective treatment for AD is early detection. You want to prevent those brain cells from being killed or dying in the first place.”

If you knew that in 10-20 years you’d develop Alzheimer’s disease, what would you do with that time? How would that affect your daily life? Share your stories with us in the comments below.

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  • willbewhatiwill

    Apparently 10 phospholipids were identified that, if present in lower than normal blood
    plasma levels, predicted with more than 90% accuracy whether an individual would go on to develop AD. All 10 are phospholipids. Though APOE4 gene, an accepted risk factor for AD, but it was not a significant predictive factor in this study. [Labmedica website; 18 Mar 2014]

    Phospholipids often form cell membranes & lipoproteins in the blood plasma and comprise of glycerol, fatty acids, phosphate groups and other organic & inorganic groups. Lipoprotein molecules enable the transportation of lipids (fats), like cholesterol, phospholipids & triglycerides, within the water around cells, including the bloodstream.

    Cholesterol rich membranes associated with Aβ appears to adopt a conformation that can act as ‘seeds’ for amyloid plaque formation.

    Low-density lipoprotein (LDL) is one of the five major groups of lipoproteins – in order of molecular size, largest to smallest, are chylomicrons, very low density lipoprotein (VLDL) intermediate density lipoprotein (IDL), LDL & high density lipoprotein (HDL).

    LDL particles (thousands of them) are often called bad cholesterol because they can transport their content of many fat molecules into artery walls, attract macrophages causing atherosclerosis. On the other hand, HDL particles (thousands of them) are frequently referred to as good cholesterol, because they can remove fat molecules from macrophages in the walls of arteries.

    Dementia & Alzheimer’s disease (AD) are different conditions. Dementia can include those
    with chronic confusion & disorientation due stroke (or other vascular disease), various physiological& genetic causes. 1 in 3 people over 65 died with dementia.

    AD are characterised by the deposition in the brain of extracellular spherical amyloid (Aβ)
    plaques& surrounded by intracellular tau tangles in the cerebral cortex,
    hippocampus, limbic system, etc.

    Healthy diets can help to prevent Alzheimer’s disease. It has been hypothesised that cholesterol can affect APP (amyloid precursor protein of Aβ) metabolism by affecting the
    activities of APP secretases & APP trafficking. Cells depleted of cholesterol had been found to also have reduced secretion of Aβ.

    Insulin can reduce tau phosphorylation to form tangles by reducing glycogen synthase kinase-3 activity. Insulin growth factor 1 (IGF-1) have been found to promote Aβ clearance from the brain.

    Cure for AD may become feasible as more & more genes (like presenilin 1&2, ApoE-four, α2
    macroglobulin) are implicated in conferring susceptibility to AD, treating AD by replacing missing gene(s) or gene products pharmacologically may become more feasible.

    Currently neuroimaging techniques detect Alzheimer’s Disease (AD) process around 3 years
    before the clinical onset of cognitive impairment – like positron emission tomography (PET), single photon emission computed tomography (SPECT), fMRI scanning can detect AD process around 3 years before the clinical onset of cognitive impairment.

    However cure AD are currently unavailable. Acetylcholinesterase (AChE) inhibitors (AChEI) can now be prescribed administered in order to INCREASE THE LEVEL OF AVAILABLE NEUROTRANSMITTERS ACETYLCHOLINE (Ach) in the brain. AChEIs do not cure but seek to treat the symptoms of decreased cognitive function & cognitive deficits.

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