16 April 2014
I have read with interest the recent report by Jin and coworkers on the putative role of SORL1 variants in sporadic Alzheimer’s disease . In their report, the authors claim a significant effect of a three-marker haplotype, but refute a second haplotype based on twenty-three case-control studies. This conclusion, it seems, is premature in view of glaring oversights.
14 April 2014
PSP-like Features without PSP Cytopathology in Three Cases of Alzheimer’s Disease/Parkinson’s DiseaseProgressive supranuclear palsy (PSP) is a progressive disabling neurodegenerative disorder manifested clinically by vertical supranucelar gaze palsy or slowing of vertical saccades, prominent postural instability, and falls. Its neuropathological substrate is 4 repeat tau deposition as neurofibrillary tangles in the basal ganglia and brainstem and tuft-shaped astrocytes.
2 February 2014
The topic of long term cognitive impairment is of concern to patients and clinicians and it is critical that it be addressed with appropriately designed studies. It is disappointing to note that despite a plethora of opinion pieces dominating the literature, there remain no prospective studies investigating dementia following surgery and anesthesia.
8 October 2013
We read with interest the article by Natunen et al.  on the role of the BACE regulating factor, GGA3, in Alzheimer’s disease (AD). In this study, as has been the case with a number of other studies [2-4], the authors utilized human postmortem brain samples to show that the temporal cortex of AD patients had decreased levels of GGA3 compared to that of age-matched controls, although the decrease was not statistically significant . In a separate study, Santosa et al.
1 September 2013
The paper recently presented by Lee et al.  impressively broadens the debate on the effects of soluble amyloid-β (Aβ) peptide oligomers applied at the cell surface of neurons and thus again fuels the question formulated in the headline. The authors, examining the impact of exogenously applied Aβ on signaling in neurons cultured on multi-electrode arrays, observed that subcytotoxic amounts of human Aβ1-42 perturbed synaptic transmissions within hours.
27 May 2013
We read with great interest the article by Moreno and colleagues . The authors should be congratulated on enlarging our knowledge on retinal nerve fiber layer (RNFL) thickness measurements in Alzheimer’s disease (AD) and other types of dementia. The results of this study show that optical coherence tomography (OCT) seems to be a useful tool for diagnosing dementia syndromes but does not seem to contribute to the differential diagnosis of different types of dementia. Nevertheless, we believe that some supplementary discussion of the problem is needed.
1 March 2013
We have read with great interest the study by Rembach and colleagues  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
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 . 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 November 2012
I read with great interest the recent article by Bai et al. . 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. This explanation is relevant within an evolutionary context. I think mammals evolved because of natural selection for dehydroepiandrosterone (DHEA) . This is based on my principal hypothesis that DHEA increases replication and transcription of DNA, that is, DHEA increases gene activation.