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  • Reply to: Dr. Oskar Fischer’s Mysterious Little Alzheimer’s Germ   3 days 4 hours ago

    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 1 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 Alzheimer’s disease (AD) and have one or more APOE-ε4 gene copies are more likely to have AD. However, APOE- ε 4 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- ε 4 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.4 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.5 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?   1 month 1 week ago
  • Reply to: Can Tau Formation be Independent of Amyloid-β in Alzheimer’s Disease?   1 month 1 week ago

    Vascular pathology as a strong predictor of cognitive decline that can act independently of amyloid pathology.

    https://www.sciencedaily.com/releases/2019/02/190205115419.htm

     

     

  • Reply to: Can Tau Formation be Independent of Amyloid-β in Alzheimer’s Disease?   1 month 1 week ago

     I am sorry that Dr. McGeer has not read my Letter carefully. I have not given information just on mouse studies, but also on human beings with AD.  To tell the truth, I was not expecting such a simple response. A detailed answer sophisticater than ' mice are not men ' would have been appreciated.

  • Reply to: Alternating Assignment was Incorrectly Labeled as Randomization   1 month 2 weeks ago

    We carefully read the Letter to the Editor by Hannon et al., which related to our previously published article [1], and checked our procedure of clinical trial. Then, we noticed that the method for participant allocation was incorrectly described. In the article, we described that “participants were assigned to the AS or placebo group using an alternating quasi-randomization allocation method” in the MATERIALS AND METHODS section. However, we actually performed “non-alternating quasi-randomization allocation method”, not to allow the controller, other researchers, and physicians to know which group the next participants would be assigned, as Hannon et al. recommended. We also checked our primary results, and confirmed that the statistical significance and graphical figure were correctly described.

    We appreciate Hannon et al. to give us the opportunity to be aware of our fault. We have requested that the above correction be made in our previous article.

    Naoki Itoa, Hitomi Saitoa, Shinobu Sekia, Fumitaka Uedaa, Takashi Asadab
    aPharmaceutical and Healthcare Research Laboratories, Research and Development Management Headquarters, FUJIFILM Corporation, 577, Ushijima, Kaisei-machi, Ashigarakami-gun, Kanagawa 258-8577, Japan
    bMemory Clinic Ochanomizu, 1-5-34, Yushima, Bunkyo-ku, Tokyo 113-0034, Japan

    Reference
    
[1] Ito N, Saito H, Seki S, Ueda F, Asada T (2018) Effects of composite supplement containing astaxanthin and sesamin on cognitive functions in people with mild cognitive impairment: A randomized, double-blind, placebo-controlled trial. J Alzheimers Dis 62, 1767-1775.

  • Reply to: Can Tau Formation be Independent of Amyloid-β in Alzheimer’s Disease?   1 month 2 weeks ago

     

    The letter from Dr. Umur Kayabasi is an excellent example of the age-old adage “mice are not men”. He claims, based upon mouse models, that there is “evidence showing that Alzheimer disease (AD) is a disorder that progresses through tau pathology, not amyloid beta protein (Abeta) pathology. However, the histological evidence from post mortem AD tissue is that it is Abeta deposits, and not tau deposits that specifically characterize AD pathology.  Although tau deposits do occur in AD, they also occur in a variety of other diseases known as tauopathies. The evidence of Dr. Kayabasi’s mouse models is therefore not an exclusive characteristic of AD itself. Consequently, it fails to represent evidence that AD is a tauopathy.