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. [1], 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. [1] 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
Labelling of Statistical Output of Cytoarchitecture-Defined Variables in FreeSurfer Version 6
In our recent paper, Fung et al. [1], 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. [2] and Augustinack et al. [3] found in FreeSurfer version 6.
3 February 2019
Alternating Assignment was Incorrectly Labeled as Randomization
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
Can Tau Formation be Independent of Amyloid-β in Alzheimer’s Disease?
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.
4 December 2018
Chronic Traumatic Encephalopathy
Recently, Zuckerman et al. [1] presented an interesting history of chronic traumatic encephalopathy (CTE), previously referred to as dementia pugilistica [2], beginning from Hippocrates up to recent publications, with emphasis on contact sports and American football. With regard to CTE in boxers, except for the first report of "punch drunk" [3] and a few others [4], they unfortunately did not refer to a number of other important contributions about brain damage in boxers, many of them having been mentioned previously [5].
16 August 2018
Effective discrimination with the recency ratio between Alzheimer’s disease and dementia with Lewy bodies
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.
23 April 2018
Response to McGeer et al.: Alzheimer’s Disease Can Be Spared by Nonsteroidal Anti-Inflammatory Drugs
In their recent publication, McGeer and colleagues [1] recommend a simple diagnostic test at age 55 to identify people who, as they elsewhere describe, are “fated to develop Alzheimer’s” [2], further suggesting that they could benefit from a daily dose of a generic anti-inflammatory drug for prevention. However, their paper presents no real data (positive and negative predictive values) on how the test would perform if used clinically.
19 March 2018
Is LMTM the Norwegian Blue of Alzheimer's Therapy?
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.
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