Letters to the Editor

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 [1]. 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 [2]. 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.

4 June 2015

Adverse Side Effects of Intranasal Detemir Insulin in the SNIFF Trial

Insulin signaling is impaired in Alzheimer’s disease [1]. 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 [2]. 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 [3].

19 March 2015

Non-Steroidal Anti-Inflammatory Drugs and Risk of Alzheimer's Disease

In their updated systematic review and meta-analysis, Wang and colleagues [1] 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

No Evidence for a Recessive Effect of TMEM106B rs1990622 Variant in the General Population

We read with interest the article by Hernández et al. on the TMEM106B genetic variant rs1990622 that modifies the risk for frontotemporal dementia (FTD) [1]. 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

Spinal Needles for Lumbar Puncture

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’ [1]. 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 [2]. This was based on only one study in the neurology literature, but overwhelming evidence in the anesthesiology literature [3]. We find it astounding that in 2014, cutting edge-tipped spinal needles are still being used for this purpose.

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 [1]. 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.”

20 July 2014

Response to: Coskuner and Murray (2014) J Alzheimers Dis 41, 561-574

I am writing with reference to the recent paper by Coskuner and Murray [1]. I am sorry but I find it very hard to believe that these authors were not aware of our previous research in the field of ATP and amyloid-β (Aβ) [2-4]. In this research, we show unequivocally that ATP, ATP + Mg, and ATP +Al (III) (as well as equivalent preparations using ADP and AMP) influence significantly the propensity for Aβ25-35, Aβ1-40, Aβ1-42, and amylin (IAPP) to form β sheets of amyloid under near physiological conditions.

6 May 2014

Response to: Kapila et al. (2014) J Alzheimers Dis, doi: 10.3233/JAD-132258

It was with great interest that we encountered the recent article by Kapila et al. [1]. The preclinical studies from this group have contributed significantly to our understanding of the relationship between the perioperative period and cognitive loss. However, with respect to translation, we believe that a much more cautionary note is due here than presented by the article. First, the evidence in humans that the perioperative period is linked to incident dementia is weak at best. Many contradictory clinical studies exist and there is simply no consensus at this point.

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