7 June 2016
The editorial paper by Itzhaki et al.  addresses critically important questions about the role of infection in etiology of Alzheimer's disease (AD). We believe that in addition to the evidence of infectious nature of AD that have been described in the paper, one more type of the evidence must be taken into account and routinely included in consideration of AD mechanisms.
26 December 2015
Inhalable curcumin is a potential treatment for herpes simplex virus type 1-associated Alzheimer’s disease
Herpes simplex virus type 1 (HSV-1) DNA is frequently detected in the aged brains of both normal individuals and patients with Alzheimer’s disease (AD) . In recent studies, the reactivation of HSV-1 in the brain is a potent risk factor for the development of AD . Reactivated HSV-1 can cause an increased formation and accumulation of amyloid-β (Aβ) and abnormally phosphorylated tau. Moreover, HSV-1-mediated disruption of autophagy in neurons may also contribute to the accumulation of these abnormal proteins .
21 September 2015
Further verification of the lack of correlation between Lyme disease and deaths due to Alzheimer’s disease
In 2014, O’Day and Catalano published a JAD article presenting statistical evidence that Lyme disease was not a cause of Alzheimer’s disease . A recent report by Phillip J. Baker, Ph.D., who is the Executive Director of the American Lyme Disease Foundation, has validated this conclusion using different statistical methodology and more recent data . To quote Dr. Baker, “An analysis of the data by linear regression analysis generates a correlation coefficient of 0.0753 (t= 0.262 for 12 degrees of freedom; p >0.05.
31 July 2015
Two compartment model of MSH/ACTH may be a surrogate for intranasal insulin central nervous system kinetics
4 June 2015
Insulin signaling is impaired in Alzheimer’s disease . In the SNIFF Trial, Claxton et al. have reported that long-acting intranasal insulin Detemir improves cognition for adults with mild cognitive impairment or early-stage Alzheimer’s disease . Adverse effects included mild rhinitis. In an earlier publication, Craft et al. note 8.3% nosebleeds and 16.7% rhinitis with a 20 IU intranasal insulin dose .
19 March 2015
In their updated systematic review and meta-analysis, Wang and colleagues  identified 12 cohort studies, 5 case-control studies, and 1 randomized clinical trial (RCT). Based on an aggregate measure emanating from adjusted risk and hazard ratios, they reported that, within a meaningful degree of heterogeneity, non-steroidal anti-inflammatory drugs (NSAIDs) are statistically significantly associated with a 28% reduced risk of Alzheimer’s disease (AD) in the general population.
14 January 2015
We read with interest the article by Hernández et al. on the TMEM106B genetic variant rs1990622 that modifies the risk for frontotemporal dementia (FTD) . Although the authors were underpowered to detect a significant association with FTD risk in their case-control study (n/N=146/381), the effect was concordant with the expected direction and slightly decreased in p-value under a recessive model. Similarly, meta-analysis of published data was more significant assuming a recessive effect for the rs1990622 CC genotype.
30 November 2014
We read with dismay the report ‘Feasibility of Lumbar Puncture in the Study of Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease: A Multicenter Study in Spain’ . In 2005, the Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology recommended the use of atraumatic needles for lumbar puncture . This was based on only one study in the neurology literature, but overwhelming evidence in the anesthesiology literature . We find it astounding that in 2014, cutting edge-tipped spinal needles are still being used for this purpose.
13 November 2014
We are writing this letter in reference to the recent paper by Gharbiya and coworkers titled “Choroidal thinning as a new finding in Alzheimer's disease: evidence from enhanced depth imaging spectral domain optical coherence tomography” .
13 August 2014
The lack of correlation between the incidence of Lyme disease and deaths due to Alzheimer’s disease cannot reflect the lack of involvement of Borrelia burgdorferi in Alzheimer’s dementia
I am writing this letter in reference to the recent paper by Danton and Catalano . I have read with interest their investigation based on the anticipation that “If the biological agent Borrelia burgdorferi that causes LD (Lyme disease) also causes AD (Alzheimer’s disease), then areas with the highest levels of LD should have significantly higher numbers of deaths due to AD compared to low LD areas.”