1 November 2012
Influence of GSK3β Polymorphisms on Psychiatric and Neurological Disorders: Recent Insights
I read with great interest the recent article by Bai et al. [1]. Interestingly, recent data suggests that rs334558 polymorphisms of the GSK-3β gene may influence a number of psychiatric and neurological disorders besides amnestic-type mild cognitive impairment.
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
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 November 2011
Response to: Luengo-Fernandez R et al. (2011) J Alzheimers Dis 27, 187-196
There has been extensive media coverage recently of the findings of Luengo-Fernandez et al. (2011). Dementia is indeed a costly condition. But, from examining the Supplementary Data (http://www.j-alz.com/issues/27/luengo_supplement.pdf), is it possible that the cost has been over-estimated?
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.
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