Possible Screening Tests for Alzheimer’s Disease- Part XIII

(5/22/15)- In the largest study to date, it was found that the presence of amyloid plaque on the brain can help predict the onset of Alzheimer’s disease. The findings confirmed that amyloid screening, by PET scan or cerebral spinal fluid testing, can help identify individuals who are likely to get the disease.

Two linked studies recently published in the Journal of the American Medical Association also supported the idea that beta amyloid formations on the brain are lead indicators for people who will develop AD. Data from almost 9,500 subjects on five continents shows that amyloid can appear 20 to 30 years before symptoms of dementia. The presence of the ApoE4 gene, known to increase Alzheimer’s risk, greatly accelerates amyloid accumulation.

Rik Ossenkoppele, a neuropsychologist at Vije University Medical Center in Amsterdam led the study, along with Willemijn Jansen and Peter Jelle Visser

(7/16/14)- Amyloid plaques that accumulate on the brain are thought to be one of the clues in detecting signs of Alzheimer’s disease. Although many medical experts have come to dispute this theory, these plaques have been known to accumulate on the eye retinae.

Two-company funded studies found that deposits of amyloid plaque can be detected through noninvasive eye-imaging technology. Cognoptics Inc., a closely held biotech company in Acton, Mass, focuses on the plaques detection in the lens of the eye.

CSTRO Australia, that country’s national science agency, and NeuroVision Imaging LLC of Sacramento, California, have been examining the accumulation of the plaque on the retina, in the back of the eyes. The first 40 patients in a 200 subject study showed that retinae changes correlated with amyloid plaque development in the brain.

The full study will be concluded this year, according to Shaun Frost, a researcher at CSIRO Australia.

(7/22/13)- The following note was found on the Alzheimer's News Special Issue, AAIC 2013, July 17, 2013:

"Most online tests for Alzheimer's disease are scientifically invalid and also fail on ethical standards, said a report released at AAIC. Experts rated 16 tests on scientific validity and reliability, human-computer interaction and ethical factors. Three-quarters of the tests were rated as poor or very poor for scientific validity and reliability, and all 16 received poor or very poor grades for ethical standards"

(11/20/12)- At a recent dinner party, a question was asked about Amyvid scans and Alzheimer's disease diagnosis. Frankly, we knew nothing about it, except having read certain preliminary research results. We know that it is not approved for reimbursement by the Centers for Medicare and Medicaid Services (CMS), but have heard that some private insurance companies are pre-certifying its use. Lilly is the primary company involved with amyvid. Below you will find the highlights of the prescribing information found on Lilly's site. We hope this is helpful to our readers. Readers should note that a negative result reduces the likelihood of cognitive impairment due to AD diagnosis, but it does not rule out other neurological issues..

Please see our item dated 10/1/12 below.


These highlights do not include all the information needed to use Amyvid safely and effectively. See full prescribing information for Amyvid.
Amyvid (Florbetapir F 18 Injection) for intravenous use. Initial U.S. Approval: 2012

_____________________ INDICATIONS AND USAGE______________________

Amyvid is a radioactive diagnostic agent for Positron Emission Tomography (PET) imaging of the brain to estimate ß-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer’s Disease (AD) and other causes of cognitive decline. A negative Amyvid scan indicates sparse to no neuritic plaques, and is inconsistent with a neuropathological diagnosis of AD at the time of image acquisition; a negative scan result reduces the likelihood that a patient’s cognitive impairment is due to AD. A positive Amyvid scan indicates moderate to frequent amyloid neuritic plaques; neuropathological examination has shown this amount of amyloid neuritic plaque is present in patients with AD, but may also be present in patients with other types of neurologic conditions as well as older people with normal cognition. Amyvid is an adjunct to other diagnostic evaluations (1).

Limitations of Use
• A positive Amyvid scan does not establish a diagnosis of AD or other cognitive
disorder (1).
• Safety and effectiveness of Amyvid have not been established for:
• Predicting development of dementia or other neurologic condition;
• Monitoring responses to therapies (1).

(10/1/12)-Dr. Sam Gandy, Professor of Neurology and Psychiatry at Mount Sinai School of Medicine in NYC has introduced the use of a radioactive agent, F-18 florbetapir, that binds to plaque and thus makes them detectable by use of positron emission tomography.

It is a means of detecting Alzheimer's disease. He is quoted as saying: "If you have memory loss or other symptoms of Alzheimer's and receive a positive scan, we can predict with 99 percent certainty that you have the disease. (Source: Mt Sinai Inside, Sept. 17-30).

This type of scan is only approved for those individuals who are cognitively impaired. He further states [I}f you have symptoms and your scan is negative, there is a 96 percent certainty you don't have Alzheimer's".

Keep in mind that this procedure cannot predict who will get Alzheimer's when they are free of mental or behavioral symptoms. By pinpointing the disease, researchers may be able to find new approaches to treat the cognitive decline

(7/23/02- As the incidence of Alzheimer’s disease creeps past 4 million the search continues, not only for drug interventions, but also for early indicators of the disease. The general theory being, the earlier the disease can be identified, the greater the chance for modifying progress of the disease. Technological advances (PET, SPECT, fMRI etc.) in screening for possible brain changes associated with Alzheimer’s disease seem to be within our grasp. (Changes in entorhinal area of brain may foretell the start of cognitive loss).

The screenings are very costly, and may not pick up the disease until it is at a level that would make it unlikely for treatment success. What is needed is an easy to use and inexpensive way of screening people at risk for, developing Alzheimer’s disease, the same way Pap smears are used for cervical cancer.

Stephen Curran and John Wattis have proposed using a psychomotor test, Critical Flicker Fusion Threshold Test, as a potential marker for developing Alzheimer’s disease. This "test" meets many needs including the fact that it is not age related, does not require reading, is portable, inexpensive to administer and it does not require a high level of training to administer. Curran and Wattis feel it measure cognitive changes over time.

Relative data exists on a population that has not experienced cognitive loss. Using normal controls, they had 26 individuals with Alzheimer’s disease, from eight Residential Homes, undergo the Critical Flicker Fusion Threshold Test, both in ascending and descending order.

A flickering light has a direct influence on cortical activity as measured by EEG. Recording of EEG indicates that changes have occurred in the occipital area of the brain. They are synchronous with the frequency of retinal stimulation. Asking individuals to press a button when they notice a change in a flickering light (descending) and when they notice the light starting to flicker (ascending) was used as a basis of trying to distinguish normal from Alzheimer’s diseased individuals. They found:

Critical Flicker Fusion Threshold and descending thresholds were significantly lower in patients with Alzheimer’s disease compared with normal controls, but ascending thresholds were not significantly different in the two groups. In addition, in the patient group, ascending thresholds were also significantly higher than descending thresholds and this latter finding is a reversal of the situation seen in normal elderly subjects; thus might be a characteristic feature of Alzheimer’s disease. (Curran and Wattis, 2000)

If this experiment can be duplicated in a controlled, double-blinded prospective study, this may become a way of enabling the treating physician to institute pharmacotherapies early in the course of the illness before damage to neurons are too advanced to reverse the process of cognitive decline. The search continues.

Reference: Curran S. & Wattis J. Critical Flicker Fusion Threshold: A Potential Useful Measure for the early Detection of AD. Human Psychopharmacology Clinical And Experimental 2000; 15:103-112.

A new compound that sets the brain aglow for Alzheimer's disease is being tested at the University of Pittsburgh where researchers have spent more than 12-years concocting the substance. Doctors administer the compound to patients intravenously and then place them under a PET scanner to record detailed brain images.The compound acts as a dye but passes safely from the bloodstream into the brain. Once in the brain, it attaches onto tiny fibrils of plaque, while at the same time avoiding attaching to normal tissues.

In the test that was done under the leadership of William E. Klunk, associate professor of psychiatry at the University of Pittsburgh, the front and temporal lobes of 9 patients glowed with neon-red mounds of plaque. The 5 healthy people who were used in the study showed no such glow. Further testing is needed for the compound with a time frame of 5-years being thought of as the earliest time frame for which the compound and procedure could be approved.

See: Alzheimer’s Disease Part I- Medications for Alzheimer's.
See: Alzheimer’s Disease Part II- Selegiline and AD.
See: Alzheimer's Disease Part III- Use of Gingko Biloba in memory problems of Alzheimer patients.
See: Alzheimer's Disease PartIV-Alternative Treatment.
See: Alzheimer's Disease Part V-Possible New Drugs for Alzheimer's Disease Treatment.
See: Alzheimer's Part VI -Early Diagnosis.
See: Alzheimer's Part VII -New Medication-Metrifonate
See: Alzheimer's Part VIII-Implications of Longer Life Expectancies
See: Alzheimer's Part IX-Ethical Care Principles
See: Alzheimer's Disease Part X-Estrogen and Alzheimer's Disease
See: Alzheimer's Disease Part XI-Pocket Smell Test
See: Alzheimer's Disease Part XII-MAO-B
See: Alzheimer's Disease Part XIV-Donepezil
See: Alzheimer's Disease Part XV-Cerebrolysin
See: Alzheimer's Disease Part XVI-MCI
See: Alzheimer's Disease Part XVII-Summary
See: Alzheimer's Disease Part XVIII-NO Releasing NSAIDs
See: Alzheimer's Disease Part XIX-Vitamin E
See: Alzheimer's Disease-Part XX-Clinical Trials
See: Alzheimer's Disease Part XXI-The Brain
See Dementia with Lewy Bodies- Part XXII-by Gourete Broderick
See: Alzheimer's Disease-Part XXIII-HMG
See: Alzheimer's Disease-Part XXIV-A Prequel
See: Alzheimer's Disease-Part XXV-Psychosis
See: Alzheimer's Disease-Part XXVI-Amyloid-beta Hypothesis Controversy
See: Alzheimer's Disease-Part XXVII- AD and Diabetes
See: Alzheimer's Disease-Part XXVIII - Insulin and AD


Harold Rubin, MS, ABD, CRC, Guest Lecturer
updated May 22, 2015

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