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.
6 September 2016
Diabetes has been known to affect Alzheimer’s disease (AD) adversely [1, 2]. A recent article postulated that the mechanism for this occurrence was comprised of four underlying malfunctions.
4 August 2016
We read with interest the article by Eichler et al.  that indicates that a high proportion of community-dwelling people with dementia live alone. The authors concluded that people with dementia living alone did not seem to be at an increased health risk, even if they lacked the support of an informal caregiver. We would like to comment on safety issues about living alone with dementia.
7 June 2016
The editorial paper by Itzhaki et al.  addresses critically important questions about the role of infection in etiology of Alzheimer's disease (AD). We believe that in addition to the evidence of infectious nature of AD that have been described in the paper, one more type of the evidence must be taken into account and routinely included in consideration of AD mechanisms.
26 December 2015
Inhalable curcumin is a potential treatment for herpes simplex virus type 1-associated Alzheimer’s disease
Herpes simplex virus type 1 (HSV-1) DNA is frequently detected in the aged brains of both normal individuals and patients with Alzheimer’s disease (AD) . In recent studies, the reactivation of HSV-1 in the brain is a potent risk factor for the development of AD . Reactivated HSV-1 can cause an increased formation and accumulation of amyloid-β (Aβ) and abnormally phosphorylated tau. Moreover, HSV-1-mediated disruption of autophagy in neurons may also contribute to the accumulation of these abnormal proteins .