News

Alzheimer's Criteria Angle for Earlier Diagnoses : Treatments to slow or halt Alzheimer's will be most effective before neuronal damage is done.


 

Previously, the only way to obtain a definitive Alzheimer's disease diagnosis was through brain autopsy; the presence of amyloid plaques and neurofibrillary tangles has been the key diagnostic feature. “With these strengthened criteria, we can now diagnose it in a living person.”

Documented and measurable memory deficits in the presence of at least one biomarker now correlates to the diagnosis of “probable Alzheimer's.” In addition to memory deficits, the presence of several biomarkers—structural brain changes, functional brain changes, positive amyloid imaging, spinal fluid abnormalities, or genetic markers—can strengthen the diagnosis of probable disease.

The presence of a genetic marker in this mix, especially the apolipoprotein E e4 allele, equates to a definitive diagnosis.

The work groups are now seeking feedback on the criteria. Comments can be submitted to the Alzheimer's Association Web site (www.alz.org/research/diagnostic_criteria

“By the time symptoms appear, there has already been substantial neuronal loss in critical brain areas, and it's been impossible to arrest the disease once this damage has occurred,” Dr. Morris said. “It makes great sense to intervene earlier—even before MCI—to see if we can treat with the hope of preventing disease progression.

The project was funded by the National Institute on Aging and the Alzheimer's Association. None of the physicians reported any potential financial conflicts.

The criteria may help diagnose AD before there is significant impairment, Dr. Reisa Sperling said.

Source Courtesy Alzheimer's Association/Lucy Pemoni

My Take

The Criteria Mark Our Progress

The proposal to update Alzheimer's disease diagnostic criteria will incorporate the progress made these last 20 years in our understanding of the disease. We already have a number of promising approaches to the disease that include both drug and non-drug interventions and much has been done to understand the basic biology and pathology of disease progression. Even though we have no cure and currently cannot prevent Alzheimer's disease, I prefer my patients to run toward a diagnosis rather than away from it, so I expect that these criteria will help.

With each advance in medicine, more sensitive and specific tests (i.e. biomarkers) are validated and used to diagnose and treat a wide assortment of conditions. This is now the case with Alzheimer's disease. It is the inclusion of these biomarkers in the updated diagnostic criteria that will help us arrive at a diagnosis sooner and to allow us to study a variety of drug and non-drug interventions in an attempt to modify disease progression.

Clinicians use a variety of tools to assess the patient. We use laboratory tests including blood, urine and cerebrospinal fluid, imaging studies, pathologic findings, and interpretation of the history and physical to arrive at our conclusions. The more sensitive and specific the test, the more sure we are that the diagnosis is correct. Alzheimer's disease is coming of age and if new tests move us forward, then we need to incorporate these tools into our plan of care.

Our understanding of amyloid and its toxic role in Alzheimer's disease has led to its inclusion as one of the biomarker criteria. The sophistication of our imaging studies has placed positron emission tomography (PET), targeted radiolabeling, and other imaging modalities into the equation as well. The genetic work that has been done including apolipoprotein E and tau now let us use this information as well in formulating a diagnosis.

As we wait for additional treatments to become available, the new criteria should not be burdensome to the clinician. Those interested in earlier interventions will need to understand these criteria and their application in establishing a diagnosis. We will need to judge if these biomarkers lead us down the right path to be worth the effort in case finding. If the criteria provide us with a more efficient route to therapy, the better we are at addressing the patient and family needs sooner rather than later.

ERIC G. TANGALOS, M.D., is co-director of education at the Mayo Clinic Alzheimer's Disease Research Center. He is also professor of medicine at the Mayo Clinic College of Medicine in Rochester, Minn. Dr. Tangalos is a consultant to Novartis and is on the data safety board for Eli Lilly; his wife owns stock in Johnson& Johnson, all of which have Alzheimer's disease products.

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