Letters to the Editor

1 March 2013

Response to: Rembach A et al. (2013) J Alzheimers Dis 34, 171-182

We have read with great interest the study by Rembach and colleagues [1] on the diagnostic value of serum copper (Cu), ceruloplasmin (CP), and ‘free’ Cu also named non-CP Cu, in the Australian Imaging Biomarkers and Lifestyle Study of Aging (AIBL). When discussing their results, these authors commented that some studies of ours on the relationship between serum non-CP Cu and Alzheimer’s disease (AD) [2-8] were produced in cohorts not adjusted for age and gender.

1 December 2012

Response to: Hebda-Bauer EK et al. (2013) J Alzheimers Dis 33, 407-422

Recently, numerous lifestyle factors have been described that influence the risk of dementia such as smoking, obesity, and physical exercise, or certain nutrients like selenium [1]. Another factor that has received little attention to so far, although it might be of crucial importance in the modern human environment with its increasing complexity and speed-up of daily events, is stress. Psychological stress occurs when individuals face situational demands that exceed their adaptive capacity.

1 September 2012

Testosterone and DHEA are Directly Involved in Alzheimer’s Disease

Testosterone and DHEA are Directly Involved in Alzheimer’s Disease. This explanation is relevant within an evolutionary context. I think mammals evolved because of natural selection for dehydroepiandrosterone (DHEA) [1]. This is based on my principal hypothesis that DHEA increases replication and transcription of DNA, that is, DHEA increases gene activation.

1 April 2012

Response to: Walton JR (2012) J Alzheimers Dis 29, 255-273

I read about the effects of aluminum on brain with features of aging and calcium signaling with interest [1]. The effects of aluminum on the brain in the pathogenesis of Alzheimer’s disease (AD) may play out at the blood brain barrier. Aluminum enhances the permeability of the blood-brain barrier to lipophilic substances [2] and the central part of the amyloid-β peptide (Aβ), the alpha helical antigenic folding domain of the Aβ folding peptide loop is lipophilic [3].

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

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 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.

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