Letters to the Editor

11 December 2022

Is Alzheimer’s Disease by Any Other Name Still Alzheimer’s Disease?

On November 1-2, 2022, PubMed listed over 190,000 entries for the search term “Alzheimer’s disease” (AD), with over 13,600 entries for 2022 alone [1], suggesting that this topic is highly researched by academics within the biomedical research community. In this letter, the topic of ‘tortured phrases’ [2], as applies to the term “Alzheimer’s disease”, is explored. Ultimately, the question is asked, if other terms are used to describe AD, would it still be recognized as such?

19 January 2022

Response to the commentary “The Use of Standardized Diesel Exhaust Particles in Alzheimer’s Disease Research” by Block and Kodavanti

In their commentary on the suitability of the use of standardized diesel exhaust particles (DEP) for studying the adverse effects attributed to particulate matter (PM), Block and Kodavanti [1] refer to our recent publication by Farahani et al. [2] in which we offered experimental evidence on the dissimilarities in chemical composition of these DEP to ambient PM to which populations are exposed. The specific DEP is diesel soot emitted by a forklift engine (NIST SRM 2975). Parenthetically, we are not the first study to demonstrate this observation. For instance, Braun et al.

23 March 2021

The Relationship Between Infections and Alzheimer’s Disease Is Modified by Vitamin D Status

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) [1]. 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.

26 October 2020

A Role for Mycobacterium in Alzheimer’s Disease?

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 [1] as an often-overlooked possibility towards Alzheimer’s disease (AD) genesis.

16 September 2020

Plasma amyloid-β oligomerization tendency levels are increased with age in healthy subjects

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) [1]. 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

Infection and Alzheimer’s Disease: Will SARS-Cov-2 Be Next?

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) [1]. 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 [2]. 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. [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).

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