19 March 2018
Treatment and interpretation of LMTM trial data by Wilcock and colleagues  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 . The latest trial was also apparently negative.
12 March 2018
In their excellent consensus statement regarding homocysteine and dementia, Smith et al.  made no mention of several important issues.
21 February 2018
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].
13 February 2018
Companion papers detailing a multicenter double-blind randomized placebo-controlled trial investigating the effects of hearing aids (HA) on cognitive and functional outcomes for persons with Alzheimer's disease (AD) were recently published in the Journal of Alzheimer's Disease [1,2].
2 January 2018
Regarding atrial fibrillation (AF), post-stroke cognitive impairment (PSCI), and post-stroke dementia (PSD), a recently published article in October 2017 by Chander and colleagues  reported that AF is a significant and independent risk factor for PSCI even after correction of other risk factors and that we should do follow up for patients with AF regardless of infarction type. This agrees with a meta-analysis done in 2012 . Also in a systemic review done in 2017 , stroke patients with AF have a risk of dementia which is 1.68 times compared with patients without AF.
17 November 2017
Response to Vos et al: Modifiable Risk Factors for Prevention of Dementia in Midlife, Late Life and the Oldest-Old: Validation of the LIBRA Index
To the Editor:
We would like to thank Vos and colleagues for valuable research on the topic of modifiable risk factors for dementia . However, we feel three topics need to be addressed in order to interpret the results with due nuance.
22 September 2017
Dietary factors for prevention of late-onset Alzheimer’s disease and related dementia: what is optimal?
Solfrizzi et al.  recently published a systematic review of observational studies published between 2014 to 2016 on dietary factors and late-life cognitive disorders. While the authors relayed the growing promise and potential of diet to change the course of late-onset Alzheimer’s disease and related dementia, their conclusion—that certain foods that have been thought to increase health risk are not as damaging as previously described—is not consistent with the emerging unifying concepts on protective dietary factors for Alzheimer’s disease [2-4].
23 May 2017
Siotto et al.  studied 84 patients with Alzheimer’s disease and observed that a one-unit increase in the specific activity of ceruloplasmin (the ratio of ceruloplasmin measured enzymatically to ceruloplasmin measured by immunoassay) was associated with a fall in disease risk of 89% in comparison to 58 healthy people.
28 September 2016
The brilliant film portrayal by Meryl Streep of the tone-deaf diva Florence Foster Jenkins is amplified in the historian Darryl W. Bullock's fine new book, Florence ! Foster !! Jenkins !!! the Life of the World's Worst Opera Singer (Overlook Press, New York, 2016). I offer here a scientific postulation for this striking example of "dysmusia " (or tune-deafness), of which she was quite likely cognitively unaware.
25 September 2016
Recently, Miklossy has shown Borrelia cultured from brains of Alzheimer’s disease (AD) not only grew organisms, but those organisms made biofilms, amyloid-β protein precursor (AβPP), and amyloid-β (Aβ) in vitro as well . With that observation, the major events in the pathogenesis of this dreaded disease have been made much clearer. They (major events) originate in most cases of the disease with spirochetes; Aβ, which is a constant in the disease, assumes a lesser role.