The nosologic categorization of “senile” is inaccurate and diagnostically problematic. And Alzheimer’s is only one dementia, and there are many others, currently about ten types. The problem is in identifying the individual’s precise dementia and treating it appropriately.

So if 4 million Americans have Alzheimer’s (over the age of 65), around 200,000 to 240,000 people have the young-onset form of the disease.

A Diagnostic Mystery

Overt symptoms of other dementias can mimic those of Alzheimer’s, and the beginning of any research or evaluation depends on accurate diagnosis. But, if many dementias appear to be the same, how does a clinician differentiate between each of them? Therein lies one of the problems. Has the diagnosis been shored up to ensure accuracy?

It’s important to note that Alzheimer’s disease can be definitively diagnosed only after death, by linking clinical measures with an examination of brain tissue in an autopsy.

I was the national clinical monitor for the first trial of a treatment for Alzheimer’s (Cognex), and the issue of diagnosis was of primary concern. One aspect of our clinical efforts was to collect brains from autopsies of patients with Alzheimer’s. The diagnosis came up against stark reality in one instance. An illustration would be helpful here.

A researcher was tasked with collecting brains as they became available from local healthcare/hospital facilities. His beeper alerted him each time he was to make a pick-up.

Bucket in hand, he went to a nearby facility where he was to collect several brains. The researcher was shocked when he arrived and was told they no longer had brains for him.

The reason they no longer had the brains was clear; they were infected with Creutzfeldt-Jakob disease, a highly contagious virus.

Misdiagnosed as Alzheimer’s, the brains had to be appropriately disposed of, and the autopsy room adequately disinfected. If brain surgery had been involved before the autopsy, all the surgical instruments would be discarded from future use, and the room left empty for robust cleaning. Even experienced clinicians had been led to an inaccurate diagnosis at that time.

Why the Brains Were Collected

The uncovering of the possible familial pathology of AD is highly important. Having this potential genetic transporting of the disease can be vital for families afflicted by the disease and this is where brain banks come to play.

The banks share samples and attendant demographic and clinical information with qualified researchers worldwide. Many brain banks operate as part of larger consortia that maintain virtual inventories of their combined holdings and offer a centralized portal to match tissue requests with local supplies.

Studies of family history say that if you have a close relative who has been diagnosed with Alzheimer’s disease — the most common form of dementia in older adults — your risk increases by about 30%. This is a relative risk increase, meaning a 30% hike in your existing risk. Genetic testing, however, does not mean you will develop Alzheimer’s because a relative has it.

Having the specific gene for AD (APOE4) does not mean you will develop the disease. Many other factors may be involved. The gene is not the sole determinant of the illness.

The Current State of Diagnosis

How Alzheimer’s changes the brain, both structurally and cognitively, was previously diagnosed utilizing paper-and-pencil tests and neuroimaging. The task has now been improved with newer techniques, including newer types of brain scans.

Although these brain scans, such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), to rule out other possible causes for symptomsmay be useful rule-outtechniques, they may not provide a definitive diagnosis of Alzheimer’s. Autopsy remains the most accurate form of diagnosis. But research has uncovered a newer test.

A new blood test (plasma P-tau217)shows promise of differentiating between AD and other dementias at a much earlier age. The analysis identified tau protein, the main actor in the forming of brain neurofibrillary tangles believed to be one primary cause of brain neuron loss.

The researchers stated “…these results indicate that plasma P-tau217 might be useful in the differential diagnosis of patients with cognitive impairment, and future studies need to examine how this might improve case management and treatment of patients with symptomatic AD.

Plasma P-tau217 might be especially useful at facilities with limited access to CSF or PET testing, such as in primary care and most memory clinics globally, including those in low- and middle-income countries, but assay development and validation in such settings are needed first.”

The most significant finding, perhaps, was in this blood test to specifically differentiate AD from other forms of dementias. One researcher, Dr. Oskar Hannson, of Skane University Hospital in Malmö, Sweden offered his assessment of the test.

“Levels of p-tau217 increase only in Alzheimer’s disease — and not in other dementia disorders also characterized by tau pathology — strongly indicating that plasma p-tau217 is very specific for Alzheimer’s disease.”

The blood test may signal the presence of tau long before symptoms appear, however, one company, AC Immune SA (NASDAQ: ACIU), is working on a vaccine to prevent tau formation. “Immunization with anti-Tau vaccines has become an important strategy for the treatment of AD and other neurodegenerative diseases characterized by tau pathology.”

The search continues as the numbers of those in the over-65-age group increases. Faced with this silver tsunami, the medical community is placing significant resources to both discovering AD earlier, prevent or treat it.

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