#1 New Molecular Imaging Biomarker for Early Detection, Prevention, and Treatment of Alzheimer's Disease


Alzheimer’s disease (AD) is like a crafty burglar: It quietly gains entrance and steals all that is precious from the
brain, then loiters around the scene of the crime, cleverly avoiding all means of detection while the brain slowly
deteriorates from its irreplaceable losses.

To date, no one has been able to discover the secret of the criminal’s modus operandi. In 1906, German
psychiatrist, Dr. Alois Alzheimer first lectured about the mass of plaques and tangles he noted in a microscopic
post-mortem brain tissue sample taken from his 51-year-old patient. More than a century later, however, scientists are still stymied as to what causes this devastating brain disease that was named after Dr. Alzheimer. Sadly, it’s a disease without a cure.

AD is the most common cause of dementia and the costs to the American family and economy have been
staggering. This will only worsen as the AD population in the U.S. grows from well over five million at present to
an anticipated 20 million within four decades. The cost of taking care of Americans aged 65 and older with AD is
expected to skyrocket from $172 billion to well over $1 trillion in that same timeframe.

Presently, even though clinical diagnosis of AD is quite accurate, a doctor can positively diagnose AD only after the patient has died, when brain tissue can be examined under a microscope for the distinctive plaques and tangles associated with the disease.

However, that is about to change very soon. Since the distinctive beta-amyloid plaques and tau tangles of AD are present at least a decade before dementia symptoms become evident in many patients, there is now a global hunt underway to find ways to help identify the initiation of brain damage caused by AD. This new goal of detecting dementia at its very earliest manifestation will then allow steps to be taken to protect the brain before too much damage is done so that people—and their loved ones—never have to experience the ravages of AD.

A new brain imaging compound will make this early detection possible. After being injected into the patient, AV-45, the radioactive molecular imaging compound then crosses the blood-brain barrier and binds to any beta-amyloid plaques, the tell-tale “signature” that is so characteristic of AD. Follow-up imaging by positron emission computed tomography (PET) allows doctors to effectively peer into the brain of a patient and assess it for dyed amyloid plaques.

It’s thought that AV-45 can be used as a biomarker not only for diagnosing AD but also for monitoring disease progress and drug efficacy. Once this novel compound receives its expected FDA approval in 2011, this dream could become a reality, paving the way for better ways to distinguish AD from Parkinson’s disease and other types of dementia; using it as an effective method of tracking disease progression from mild cognitive impairment to late AD; and utilizing it as a key diagnostic in the development and testing of the more than 150 AD drugs presently in the pipeline.

Over time, it’s expected that AV-45 will gradually become the dominant part of the diagnosis of AD, an important innovation that will help change the course of AD research and treatment as we now know it.

Where Are They Now

Florbetapir, the new brain imaging compound, will make early detection of Alzheimer's disease possible by identifying the initiation of brain damage. Injection of this radioactive molecular imaging compound "binds" to amyloid plaques, which is the telltale 'signature' characteristic of Alzheimer's. Follow-up imaging allows physicians to effectively peer into the brain of a patient and assess.

Florbetapir received FDA approval in 2012 for use in PET scans to detect accumulation of amyloid plaque to determine if Alzheimer’s disease is present. In a 2015 published article, physicians further analyzed the importance of this technology still in its beginning phases. The physicians cited its high additional cost to clinical trials as the overarching reason this technology has not been fully developed and integrated into common practice. Despite said cost, a four year study to determine whether or not amyloid PET scans with florbetapir change health outcomes for these patients kicked off in 2016. The projected hope in the coming years is that through inclusion in clinical trials and involvement with oncologists, radiologists and the pharmaceutical industry this technology will be further developed and implemented into surgical practice.

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