8066 RESULTS
COMMENT This is a well-thought-out hypothesis paper. It presents us with a new intellectual framework for future studies of the role of familial Alzheimer’s disease mutations in the amyloid precursor protein (APP) and presenilin genes to change iron, metal, and ...
COMMENT I really liked this study, which elegantly combines work in human and transgenic tissue, in vitro and in primary cultures. The human brain and doxycycline rescue experiments in rTg4510 mice are especially compelling. I think the question (admittedly a ...
COMMENT In this paper, Kiaei and colleagues have taken a unique approach to investigate how mutations in the profilin gene affect the three-dimensional structure of the protein and its interaction with binding partners. This study, even though mainly performed in ...
COMMENT Here the authors did a systematic analysis of Toll-like receptor (TLR) gene expression in the brains of AD patients versus controls and they found a significant increase in specific members of this family, including TLR2, 4, and 5. To explore the role of ...
COMMENT Rumors that physical exercise might be able to counteract dementia (and also major depressive disorder, MDD) in a BDNF-dependent fashion have been rife in the field for more than 10 years. Nevertheless, a causal connection between physical exercise ...
COMMENT This paper and others recently published (see below) illustrate the critical role played by APP in the regulation of cellular iron homeostasis. APP translation is controlled by the binding to its mRNA of Iron Regulatory Protein 1 (IRP1). Using SH-SY5Y ...
COMMENT This study represents a landmark achievement, in that PET data acquired with the most widely used tau tracer have now been compared on an individual basis with postmortem findings in 67 participants. As was the case with amyloid PET, the Avid team has led ...
COMMENT The mechanism of how PFN1 mutations cause familial ALS is still unclear, but these mutations are autosomal-dominant and mutants are destabilized and prone to form aggregates (Boopathy et al., 2015). Therefore, gain of toxic function of mutant PFN1 would ...
COMMENT I think this is a carefully executed study that combines chemical and viral approaches to deliver neurogenic factors into the hippocampus for amelioration of cognitive decline and amyloid pathology in an established mouse model of β-amyloidosis. This is ...
COMMENT This is a very complex study, looking at how physical exercise might build protective effects against cognitive impairment in a genetic model of AD. The idea is that adult hippocampal neurogenesis plays a central role, at least as far as the hippocampus ...
COMMENT Nucleocytoplasmic transport of molecules is essential for normal cell function. It is, in my opinion, the most basic and fundamental processes that initiate a cascade of events that leads to cellular aging and cell death. The mislocalization of molecules ...
COMMENT This study is enchantingly novel and interesting. Before getting into the concepts, some acknowledgment is appropriate for the ingenuity of the experimental approach as well as for the creativity of the underlying research question. The authors started ...
COMMENT It was very interesting to see the range of studies around immunodetection of neurofilament proteins in blood in the context of Alzheimer’s disease, made possible by sensitive new SIMOA techniques developed at the University of Gothenburg. While this is ...
COMMENT In the study by Ludtmann et al., 2018, we reported the effect of the oligomeric conformation of α-synuclein on mitochondrial function, and its interaction with ATP synthase in two systems: exogenous application of recombinant protein aggregates to primary ...
COMMENT These [11C]Martinostat PET studies are nicely executed, informative, and potentially useful for future CNS drug-discovery pursuits when studying target engagement, etc. However, they do not help validate/invalidate HDACs as drug targets for AD or any ...
