Letters to the Editor

1 February 2012

Response to: Zhou JW et al. (2012) J Alzheimers Dis 28, 471-480

It is important to clarify, based upon the data presented, this paper’s conclusion that cathepsin B lacks “β-secretase activity” because the ambiguity of that statement could lead some readers to erroneously believe that the data show cathepsin B lacks the wild-type (WT) β-secretase activity that predominates in the common form of sporadic Alzheimer’s disease (AD).

1 January 2012

Follow-up clinical data from Tzimopoulou S et al. (2010) J Alzheimers Dis 22, 1241-1256

We would like to make you aware of follow-up clinical data from an open-label extension (OLE) study (AVA104617) to the rosiglitazone positron emission tomography (PET) study 49653/461, which was recently published [1]. The complex and technical nature of the PET study and the need to present results in a comprehensive fashion precluded the inclusion of these open-label data in the original manuscript. Therefore we are making the following information available to your readers.

1 December 2011

Possible Alteration of Amyloid-β Protein Precursor Metabolism or Trafficking in a 17β-Hydroxysteroid Dehydrogenase X Deficiency Patient

We read with great interest the recent report by Ortez et al. [1], “Undetectable levels of CSF amyloid-β (Aβ) peptide in a patient with 17β-hydroxysteroid dehydrogenase deficiency”. The authors claim that Aβ peptide was not detectable in the cerebrospinal fluid (CSF) of a mentally retarded patient. The dramatically reduced levels of amyloid-β peptide in CSF might indicate an alteration of amyloid-β protein precursor metabolism or trafficking in the patient’s brain.

1 December 2011

Response to: Dobos N et al. (2012) J Alzheimers Dis 28, 905-915

I read with interest the recent article by Dobos et al. [1] on the role of indoleamine 2,3-dioxygenase (IDO) in depression (MDD), suggestive of overlaps to the role of IDO in Alzheimer’s disease (AD). The kynurenine pathways are an area of extensive current research, given the links to stress, prodromal MDD, emergent seizures, and neurodegeneration [2]. I wondered as to whether the authors had considered a role for the aryl hydrocarbon receptor (AHr) and circadian genes in the regulation of IDO.

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.

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