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Screening for Dementia: A Cautionary Tale Yet to Begin

3 Mins read

Posted in Clinical EducationHealthcare Policy & The MediaScience & Research

Posted in Clinical EducationHealthcare Policy & The MediaScience & Research

First a disclaimer from the principal investigators: …he and other researchers took pains to emphasize that their work shouldn’t necessarily worry everyone who’s ever had a memory glitch.

Now, for the concern, or, rather pre-hysteria. If you think you have Alzheimer dementia, then you just might. Headlines containing reader-baiting ledes like this are littering the Internet today and occupying top-story real estate on many sites. Researchers in many centers throughout the world are releasing data that appear to be shedding light on the incidence of early cognitive deficit as prime risk for the development of full blown dementia. Several online media outlets have cited trials from here, here, here, and here as essentially being prima facie evidence that anyone who feels as though his or her memory is failing may be irrevocably coasting on the road to developing dementia — helpless without a known cure in sight.Image

This moment brings to mind the existence of a serologic test — the presence of the ApoE ε4 variant of ApoE, the gene with strongest association with Alzheimer dementia development — and its discovery in 1993 that created concern in a poorly informed populace over its status as a predictor for the diagnosis of Alzheimer dementia in susceptible individuals. Never mind that no causation has been ever established between this gene, its variant, and the eventual diagnosis of AD — it was, and probably still is, just enough to sell it as a “significant risk factor for AD development”. In academic research settings, the presence of this genetic material has shown rich promise in those who have a parent with AD. Having inherited a single ApoE ε4 variant increases one’s risk of developing AD by a factor of three in men and four in women, and having two copies increases risk up to 15-fold compared to persons without the ε4 variant. There was a reason for the search and identification of this gene — the presence of deterministic mutations in the human genome (much rarer breeds, indeed) could be compared to ApoE, a so-called susceptibility polymorphic gene. The presence of one or two ε4 alleles increases the risk but does not guarantee that someone will develop AD. Almost all deterministic mutation carriers develop mid-life AD, but many people with ApoE ε4 do not. Conversely, many people who have AD carry no ApoE ε4 gene variant. Case closed, right? Not so fast.

Of course, the challenge lies in explaining what all of this means to the average patient — a daunting task for any specialist in neurology, psychiatry, or god forbid — primary care. Why would a patient want to have this testing when they may or may not have concerns about their memory or cognition? After all, when a patient has no history of a deterministic genetic mutation heralding certain development of some dreaded disease, the patient has to prepare himself or herself for a positive finding — the requirement of the clinician to adequately interpret such testing, notwithstanding. I don’t know about you but, I don’t know many docs who have the time or energy to struggle with the concepts of graded risk and interpretation of probabalistic risk assessments to come up with a nice, neat answer on one’s likelihood of developing AD, complete with a bow on top. We were counseled by several advocacy organizations, perhaps mercifully so, to discuss genoptypic testing like this within the spin of helping patients cope with patients who clearly had cognitive impairment place their diagnosis into perspective, acknowledging its place within the bigger picture of estate planning, long-term care issues, and general planning purposes. Certainly, ordering genotypic analysis was not for diagnosis. But what about PET scanning, memory testing, and the green light the media have apparently given patients to demand such testing when they show the slightest cognitive deficit?

If we generalize examples such as these within the scope of preventive care, the cost of delivering that care, the potential explosion of access to (primary) care under the ACA, and the sheer numbers of Boomers with memory concerns — where will the depth of all of this testing and counseling among the worried well and sick among us alike actually take us? Is all of this education for the compliant healthcare consumer beneficial? Or is it really hysteria? We must remember that treatment of AD — a disease with no cure — is among the costliest within the healthcare marketplace, and everyone who has had a “memory glitch” is fair game when they come asking a provider to evaluate their concerns … assuming there are enough providers to meet that demand, and enough money to pay for its consequences. |

(diagnosing dementia / shutterstock)

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