23 March 2021
A forthcoming article in the Journal of Alzheimer’s Disease reported that having a burden of infectious disease was associated with a small increase in the risk of Alzheimer’s disease (AD) (OR, 1.05; 95% CI, 1.02 to 1.08) . They found significantly increased associations for bacterial infections but not viral infections. A reasonable question is whether the associations are caused by the infection or are, perhaps, related to an underlying factor that is a risk for both the infections and AD. The underlying factor considered here is vitamin D status.
28 February 2021
26 October 2020
We looked forward to Lowry’s “Alzheimer's disease: protective effects of Mycobacterium vaccae, a soil-derived mycobacterium with anti-inflammatory and anti-tubercular properties, on the proteomic profiles of plasma and cerebrospinal fluid in rats” publication in the Journal of Alzheimer’s Disease  as an often-overlooked possibility towards Alzheimer’s disease (AD) genesis.
16 September 2020
We have well received the research published by Youn et al. that reports the potentiality of plasma amyloid-β (Aβ) oligomerization levels as a diagnostic biomarker in Alzheimer’s disease (AD) . Many studies have claimed that there is a positive correlation between the risk of AD and plasma oligomeric Aβ (OAβ) levels [2-4]. Generally, the prevalence of AD increases with age, which leads to the hypothesis that the occurrence of cases with higher levels of plasma oligomerization tendency level increases with age.
4 August 2020
We read a commentary by Naughton and colleagues published in your journal with extreme interest regarding the potential novel role of Coronavirus Disease-19 (COVID-19) in Alzheimer’s Disease (AD) . In addition, we also read a review by Fotuhi and colleagues in this journal, the neurological complications triggered by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-Cov-2) and the possible mechanism of the connection between SARS-Cov-2 and the brain . Their views are inspiring for neurologists who are concerned about the neurodegenerative diseases following COVID-19.
14 June 2020
Letter to the Editor: Comment on “Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer’s Disease-like Pathophysiology in APP/PS1 Mice"
This letter refers to the article “Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer’s Disease-like Pathophysiology in APP/PS1 Mice” by Fuchsberger et al. , reporting that oral administration of MSG accelerated the onset of pathophysiological and behavioral symptoms in APP/PS1 mice, a genetically modified animal model of Alzheimer’s disease (AD).
6 September 2019
Comment on Reliability and validity of the Chinese version of the Mild Behavioral Impairment Checklist for screening for Alzheimer’s disease
I read with interest the study of Cui et al.  assessing the reliability and validity of the Chinese version of Mild Behavioral Impairment-Checklist (MBI-C) in Alzheimer’s disease (AD) patients. The authors address key elements of the validation process, but their conclusions—the Chinese MBI-C is high in validity and reliability as well as superior to Neuropsychiatric Inventory Questionnaire—are unfortunately weakened by some persistent misconceptions of scale validation in general, and some common issues in neurodegenerative disease research.
14 March 2019
In our recent paper, Fung et al. , we investigated the validity of automated FreeSurfer protocols in a group of routine clinical brain MRI scans. One structure of interest was the entorhinal cortex, in which we compared manual segmentation against automated segmentation generated by the ex vivo protocols of Fischl et al.  and Augustinack et al.  found in FreeSurfer version 6.
3 February 2019
A Letter Regarding “Effects of Composite Supplement Containing Astaxanthin and Sesamin on Cognitive Functions in People with Mild Cognitive Impairment: A Randomized, Double-Blind, Placebo-Controlled Trial”
3 February 2019
I read the article on the possibility of sparing Alzheimer’s disease (AD) by nonsteroidal anti-inflammatory drugs  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.