Letters to the Editor

I read the article on the possibility of sparing Alzheimer’s disease (AD) by nonsteroidal anti-inflammatory drugs [1] with great interest. It is stated that AD is characterized by the start of amyloid-β (Aβ) deposition in brain with consequent decreases in the cerebrospinal fluid (CSF), and therapeutic opportunities at this initial stage are at their highest. It is also stressed that biomarker studies suggest that phase 2 (Braak staging) sets in about 5 years later.

Despite neuropsychological differences between individuals with Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB), overlap in performance has been observed, including analogous scores in memory tests (Rey Auditory Verbal Learning, AVLT; e.g., [1]). All the while, differential diagnosis remains a costly exercise.

Treatment and interpretation of LMTM trial data by Wilcock and colleagues [1] is reminiscent of the Monty Python sketch in which the demise of an obviously dead parrot is disputed by a desperate shop owner who describes it as merely resting, stunned or pining for the fjords. This phase 3 trial of 18 months' treatment in patients with mild Alzheimer's disease (AD) followed a 15-month study in mild to moderate patients that showed no treatment benefits for LMTM [2]. The latest trial was also apparently negative.

I recently attended the Annual Mild Cognitive Impairment Symposium in Miami, where a presentation on the future treatment of dementia focused solely on pharmaceuticals. As a psychopharmacologist, I was familiar with the data. I questioned why the presenter did not include Functional Medicine (FM, a translational medicine approach which converts preclinical research into clinical treatments for chronic diseases) in the future of MCI and AD treatment, since efficacy has been documented in early studies [1,2].