1 October 2011
Response to: Zhang RY et al. (2011) Clinical Trials 8, 5-14
Critical for the increasing prevalence of Alzheimer’s disease and mild cognitive impairment are treatments that modify disease progression rather than providing only symptomatic benefit.
1 August 2011
Response to: Chen M et al. (2011) J Alzheimers Dis 24, 3-10
I read with interest a recent article by Chen et al. [1] in the Journal of Alzheimer’s Disease (JAD) where the authors review various concepts relating to the possible cause of Alzheimer’s disease (AD). In that paper, Dr. Chen states: “Thus, put together we propose that advanced aging plus risk factors best explain most SD (senile dementia) cases (4)”. That reference “(4)” cites Dr. Chen’s previous paper from Frontiers in Bioscience published in 2001. In that Frontiers article, Dr.
1 May 2011
Response to: Lescai F. et al. (2011) J Alzheimers Dis 24, 235-245
We have read with interest the paper of Lescai et al. We were quite surprised by the lack of any reference to a previous study of Bizzarro et al., already reporting these results. In a relative large sample of AD cases from Central and Southern Italy Bizzarro et al. observed a significant association of the -219 (rs405509) polymorphism with AD. Similar, an association of the -219/e4 haplotypes with AD was also reported. Therefore, the study of Lescai et al.
1 February 2011
Could a Combination of the Clock Drawing Test and the Mini-Mental Status Examination Be Used to Screen Dementia in a Neurological Setting? Comments with Data from the NEDICES Survey
The interesting paper recently presented in the Journal of Alzheimer’s Disease [1] suggests, in agreement with one recent report [2], a utilization of the clock drawing test (CDT), in combination with the Mini-Mental Status Examination (MMSE), as a screening method for Alzheimer’s disease (AD) and mild cognitive impairment (MCI) in a neurological setting. This is a relatively new use of the CDT and MMSE, because both tests are traditionally and preferably employed in these disorders in population- and community-based surveys [3].
1 December 2010
Aluminum may cause hyperphosphorylation of tau and result in aberrant dislocation to dendrites
The article by Walton [1] indicated aluminum is instrumental in causing hyperphosphorylation of tau with subsequent development of neurofibrillary tangle formation. Recently tau has been found to mislocalize to dendritic spines causing early synaptic dysfunction [2]. Aluminum mediated hyperphosphorylation of tau may be a trigger for tau dysfunction and abnormal cellular trafficking with mislocalization to dendrites causing synaptic dysfunction, which probably is an early feature of Alzheimer's disease.
1 May 2010
Response to: Perucho J et al (2010) J Alzheimers Dis 19, 1245-1259.
We note that Perucho et al. [1] cite (reference number 28) a 2007 publication by Pravat K Mandal [2], and we wish to point out to the authors and your readers that the Biochemistry paper in question was retracted later that same year [3], as was another article by Mandal [4], because “the anesthetic concentration of our paper[s] was misrepresented”. Those papers should therefore not be cited as evidence.
1 May 2010
Regarding Article: Arendash GW et al. (2010) J Alzheimers Dis 19, 191-210
We thank Dr. Kumlin and colleagues for their insightful comments regarding our paper [1]. Inasmuch as we were unaware of their earlier study involving EMF exposure to normal rats [2], we did not include it among the references in our paper and apologize for this oversight. Kumlin et al. [2] did indeed provide initial evidence that long-term EMF exposure (2 hrs/day, 5 days/week, for 5 weeks) can improve cognitive performance in rodents. It is important to note, however, that they provided EMF exposure to very young rats from 3-8 weeks of age.
1 April 2010
Response to: Zhang LJ et al. (2010) J Alzheimers Dis 19, 849-858
In a recent issue of Journal of Alzheimer’s Disease, Zhang and colleagues presented interesting data concerning the cholinergic deficit in Alzheimer’s disease (AD) [1]. These results demonstrated decreases in the activity of acetylcholinesterase (AChE) and reduced mRNA levels of α4 and β2 nicotinic acetylcholine receptor (nAChR) subunits in peripheral blood of patients with AD in an elderly Chinese population.
1 March 2010
Response to: Sorensen A (2009) J Alzheimers Dis 16, 451-465
To the Editors, Like many with an interest in the field of Alzheimer’s disease I was intrigued to read the recent paper in JAD which purported to report the ‘scientific productivity and impact of the top 100 investigators in the field’ [1]. As an outsider to the study of ‘scientometrics’ it appeared a thorough piece of work though there were few indications as to its actual aims.
1 March 2010
Response to: Arendash GW et al. (2010) J Alzheimers Dis 19, 191-210
A very interesting article by Arendash et al. (1) was published in the January 2010 issue of Journal of Alzheimer’s Disease. The results suggested that exposure to radiofrequency (RF) radiation similar to that emitted by mobile phones may provide cognitive benefits both in normal mice and in a transgenic mouse model of Alzheimer’s disease (AD).
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