When it comes to Alzheimer’s disease (AD) nothing is simple, not even counting how many persons are succumbing to it. Using information from death certificates investigators noted an apparent substantial increase in AD mortality between 1999 and 2014 (1, 2). This work is significant, but death certificate studies have some unavoidable limitations. One issue is that it only reveals a fraction of the actual AD cases. In addition, a formal diagnosis of AD requires post mortem neuropathologic confirmation and determinations based solely on clinical findings may confuse AD with other dementia-producing conditions. Despite the problems, the death certificate study comports with prior work suggesting AD is a big, and growing, public health menace.
Just over a year earlier reports emerged that dementia incidence was apparently dropping in some areas (3). The findings encouraged us to believe it might be possible to stave off or prevent AD by controlling blood pressure, managing diabetes and encouraging healthy, active lifestyles. Which reports should we believe? Remarkably, it is possible that AD could be increasing while at the same time dementia could be decreasing in some situations. The complication may reflect the fact that AD and dementia are different animals. In fact, there are many biochemically distinct routes to brain malfunction and AD happens to be the most common of them. AD subjects harbor abnormal deposits of amyloid-β peptides and tangles formed of the microtubule-associated protein tau. However, other forms of dementia are linked to large deposits of tau alone, molecules such as α-synuclein or damage to the brain vascular system. In fact, this complexity has confounded clinical trials of possible AD treatments. The clinical signs and symptoms of dementia produced by different biochemical pathologies overlap which makes them hard to distinguish. If you want to cure AD, but 20-30% of your demented trial participants actually have another type of unrelated dementia, it can be challenging to detect a beneficial impact from your treatments. New imaging methods are now helping investigators better sort out prospective study subjects. Again, with AD, simple answers are elusive as these new imaging protocols have also revealed our standard ideas as to how AD begins may need to be revamped.
Perhaps the biochemical diversity of dementia allows us to rationalize how AD could be increasing while dementia might be decreasing in some circumstances. Not all dementias come about in the same way and some may be more amenable to mitigation by managing lifestyle, diet or other interventions such as controlling blood pressure. The bottom line is that dementia is a clinical finding, but most of the time no one is really sure what pathological changes in a particular patient’s brain have conspired to produce it. The situations culminating in dementia are varied and complex. AD is but one of many brain pathology-producing beasts scientists are attempting to subdue.
(1) G. D. Zakaib. 2017. Alzheimer’s Deaths on the Rise. Alz Forum, 27 May 2017. http://www.alzforum.org/news/research-news/alzheimers-deaths-rise
(2) C. A. Taylor et al. 2107. Deaths From Alzheimer’s Disease – United States, 1999-2014. Morbidity and Mortality Weekly Report 66(20):521-526, https://www.cdc.gov/mmwr/volumes/66/wr/mm6620a1.htm
(3) B. Rogers. 2016. Dementia Incidence in Britain Dropped, Mostly in Men. Alz Forum, 21 April 2016. http://www.alzforum.org/news/research-news/dementia-incidence-britain-dropped-mostly-men
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