Reply to: Tau Biology, Tauopathy, Traumatic Brain Injury, and Diagnostic Challenges.
Very important question in the field
Reply to: Comment on Reliability and validity of the Chinese version of the Mild Behavioral Impairment Checklist for screening for Alzheimer’s disease
We have carefully read the Letter to the Editor by Toni T. Saari, who made some proposals for our recently published article. We have checked the calculation method of internal consistency reliability and construct validity respectively, and provide the following feedback.
As the authors say, alpha increases with the number of items, and the great Cronbach’s alpha coefficient of the whole scale may be related to the big number of items. We have also calculated the alpha of each subscale and got nice results in most of the dimensionalities. Only one coefficient is just fair (greater than 0.6 and less than 0.7), and the reasons for this are clearly explained in the discussion. There are indeed some studies showing that there are many better alternative methods to replace the Cronbach’s alphas to calculate the reliability of the scale; in particular, omega is more suitable for the scale with multidimensional and tau non-equivalence. However, it is also mentioned in many studies that, due to the lack of tau equivalence, compared with omega, Cronbach’s alpha tends to underestimate rather than overestimated the reliability of the scale [1-3]. Nowadays, the Cronbach’s coefficient is still the most widely used method of reliability calculation.
In addition, we have always acknowledged that the construct validity of the study results is not ideal, which may be related to the selection of the subjects and cultural differences. We also hope to expand the sample size to calculate confirmatory factor analysis in the further study, for optimizing the scale items. Although the content validity and criterion validity of the scale are good, the conclusion that the Mild Behavioral Impairment-Checklist (MBI-C) has high reliability and validity is still not accurate and easy to cause misunderstanding. Because the construct validity is not ideal, it is indeed unprecise to draw this conclusion directly.
We appreciate Professor Toni T. Saari’s attention to our research and for making useful suggestions. This study aims to explore whether MBI, as a new scale for testing behavioral impairment, can replace the Neuropsychiatric Inventory Questionnaire to be an effective tool for screening patients with Alzheimer's disease (AD). Although the small sample is the limitation of this study, MBI-C still demonstrates its superiority of screening. Considering that the internal consistency of each dimensionality of the scale and the structural validity are not ideal enough, we would like to accept the professor's suggestion sincerely, and modify the research conclusion as "This study showed that the Chinese version of the MBI-C has good reliability and validity, and could be used as an alternative scale to the NPI-Q for AD dementia screening in the Chinese population, but further large sample studies to inspect its construct validity is necessary". We hope to make up for the shortcomings of this study in further studies, and still believe that the MBI-C has a good implementation prospect in the screening of patients with AD in China.
Yue Cui, Fang Li, and Liyong Wu
 Deng L, Chan W (2017) Testing the difference between reliability coefficients alpha and omega. Educ Psychol Meas 77, 185-203.
 Peterson RA, Kim Y (2013) On the relationship between coefficient alpha and composite reliability. J Appl Psychol 98, 194-198.
 Tavakol M, Dennick R (2011) Making sense of Cronbach's alpha. Int J Med Educ 2, 53-55.
Reply to: Dr. Oskar Fischer’s Mysterious Little Alzheimer’s Germ
Recently, several mentions on the internet have been made that early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.
Actually, this is historically inaccurate:
Dr. Oskar Fischer1 linked Alzheimer's to the germ called Streptothrix, an older designation for the disease Actinomycosis, although an association between Fischer's Streptothrix and tuberculosis has recently been implied.2References1. Fischer O, “Miliare Nekrosen Mit Drusigen Wucherungen der Neurofibrillen, eine Regelmassige Veranderung der Hirnrinde bei Seniler Demenz,” Monatsschr f Psychiat Neurol 22 (1907): 372; O. Fischer, “Miliary Necrosis with Nodular Proliferation of the Neurofibrils: A Common Change of the Cerebral Cortex in Senile Dementia,” Monatsschrift fur Psychiatrie und Neurologie, vol. XXII, Th. Ziehen (ed). (Berlin: Karger, 1907), 361–72; In The Early Story of Alzheimer’s Disease, edited by Katherine Bick, Luigi Amaducci, and Giancarlo Pepeu (Padova: Liviana Press, 1987), 5–18.
2. Broxmeyer L. Alzheimer's Disease –How Its Bacterial Cause Was Found and Then Discarded. CreateSpace Independent Publishing Platform (August 3, 2016). 190 pages. ISBN-10: 1491287357 ISBN-13: 978-1491287354. https://tinyurl.com/ycoo233n
Reply to: A Clinicopathological Investigation of White Matter Hyperintensities and Alzheimer's Disease Neuropathology.
Important paper. Very useful
Reply to: Dr. Oskar Fischer’s Mysterious Little Alzheimer’s Germ
Dr. Lawrence Broxmeyer MD1* and Dr. George Perry PhD2
1 Chief Scientist of the New York Institute of Medical Research, USA
2 Professor and Chief Scientist of the Brain Health Consortium. Semmes Foundation Distinguished University Chair in Neurobiology, the University of Texas at San Antonio (UTSA)
As in the case of other CNS infectious agents claimed to cause Alzheimer’s disease (AD), the theory that Herpes Simplex Virus or any other herpes virus causes AD is still controversial. In their 2013 review, Mawanda and Wallace’s Can Infections Cause Alzheimer’s Disease  gave seven annotated references as to why HSV-1 “remains questionable” as a cause for Alzheimer’s. Some say that Herpes simplex virus type 1 in conjunction with APOE-epsilon 4 allele is a strong risk factor for AD, though either of these features alone do not increase the risk for AD. It is claimed that people who have symptoms of late onset AD and have one or more APOE-ε4 gene copies are more likely to have AD. However, APOE-ε4 is not diagnostic of AD and should not be used to screen people or their family members. Furthermore, many of those who have e4 alleles will never develop AD. And even in symptomatic people, only about 60% of those with late onset AD will have APOE-ε4 alleles [2,3]. Not only is the APOE gene not a clinical diagnosis, but just as importantly, “negative” results do not confer later protection. Beyond APOE, there are at least 20 other genetic factors which have been shown to have a small but significant role in determining Alzheimer risk . And true understanding of genetic test results also requires attention to potential inaccurate results. For example, APOE-ε4 alleles themselves are known to show a distinct increase in tuberculosis . Before widespread institution of anti-herpetics is unleashed on the general population, this is an area which requires further research.
Citation: Lawrence Broxmeyer and George Perry. “Alzheimer’s Disease: Questions Raised by a Herpes Virus Origin”. Current Opinions in Neurological Science 3:2 (2019): 652-660. DOI: 10.5281/zenodo.2592845.
PDF available at: https://zenodo.org/record/2592845
Reply to: Can Tau Formation be Independent of Amyloid-β in Alzheimer’s Disease?
The Zebrafish are not Men , either :